Nutrient chapter

Biotin

Vitamin B7; substrate for multivitamin transport and cofactor precursor for carboxylases.

110 recorded mechanisms · 27 availability situations · 5 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

HLCS activates biotin with ATP to form enzyme-bound biotinyl-5-prime-AMP before transferring biotin to a carboxylase acceptor.
Human holocarboxylase synthetase / HLCS → Biotinyl-5-prime-AMP source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/19740736.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d785655901465bc9798378986d954b87111e3bd73d6877d9d60ae3d95cac0a37", "start_char": 2587, "end_char": 3080, "text_sha256": "fa0ec838311a45e8ccebf38a73e340a46417eae6bc300064c1165a4a0b711889"}
experimental_model
Purified full-length and residue-58 human HLCS isoforms expressed in E. coli
exposure
Biotin/ATP activation and single-turnover biotin transfer
limitations
Minimal-substrate kinetics do not prove a universal tissue allocation hierarchy; expression host is not the protein species.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Biotin must first be activated before it can be attached to an enzyme.
primary_references
[b7-p19740736] Distinct amino termini of two human HCS isoforms influence biotin acceptor substrate recognition. (2009). https://pubmed.ncbi.nlm.nih.gov/19740736/ DOI: 10.1074/jbc.m109.046201
tissue_or_cell_type
Purified proteins and minimal biotin-accepting substrate
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 351–362
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified full-length and residue-58 human HLCS isoforms expressed in E. coli · source_derived_draft · unverified_draft
### b7-hlcs-adenylation HLCS activates biotin with ATP to form enzyme-bound biotinyl-5-prime-AMP before transferring biotin to a carboxylase acceptor. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Biotin must first be activated before it can be attached to an enzyme. organism: Homo sapiens tissue_or_cell_type: Purified proteins and minimal biotin-accepting substrate experimental_model: Purified full-length and residue-58 human HLCS isoforms expressed in E. coli limitations: Minimal-substrate kinetics do not prove a universal tissue allocation hierarchy; expression host is not the protein species. exposure: Biotin/ATP activation and single-turnover biotin transfer evidence_span: {"source_cache": "artifacts/biotin-research/19740736.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d785655901465bc9798378986d954b87111e3bd73d6877d9d60ae3d95cac0a37", "start_char": 2587, "end_char": 3080, "text_sha256": "fa0ec838311a45e8ccebf38a73e340a46417eae6bc300064c1165a4a0b711889"} [b7-p19740736] Distinct amino termini of two human HCS isoforms influence biotin acceptor substrate recognition. (2009). https://pubmed.ncbi.nlm.nih.gov/19740736/ DOI: 10.1074/jbc.m109.046201
Complete structured claim and evidence
HLCS transfers the activated biotin moiety to the epsilon-amino group of a specific lysine in a carboxylase biotin-acceptor domain.
Human holocarboxylase synthetase / HLCS → Protein-bound lysine residue source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/19740736.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d785655901465bc9798378986d954b87111e3bd73d6877d9d60ae3d95cac0a37", "start_char": 2587, "end_char": 3080, "text_sha256": "fa0ec838311a45e8ccebf38a73e340a46417eae6bc300064c1165a4a0b711889"}
experimental_model
Purified full-length and residue-58 human HLCS isoforms expressed in E. coli
exposure
Biotin/ATP activation and single-turnover biotin transfer
limitations
Minimal-substrate kinetics do not prove a universal tissue allocation hierarchy; expression host is not the protein species.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Biotin becomes a tethered part of the enzyme; free lysine and enzyme-bound lysine are different entities.
primary_references
[b7-p19740736] Distinct amino termini of two human HCS isoforms influence biotin acceptor substrate recognition. (2009). https://pubmed.ncbi.nlm.nih.gov/19740736/ DOI: 10.1074/jbc.m109.046201
tissue_or_cell_type
Purified proteins and minimal biotin-accepting substrate
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 364–375
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified full-length and residue-58 human HLCS isoforms expressed in E. coli · source_derived_draft · unverified_draft
### b7-hlcs-lysine-transfer HLCS transfers the activated biotin moiety to the epsilon-amino group of a specific lysine in a carboxylase biotin-acceptor domain. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Biotin becomes a tethered part of the enzyme; free lysine and enzyme-bound lysine are different entities. organism: Homo sapiens tissue_or_cell_type: Purified proteins and minimal biotin-accepting substrate experimental_model: Purified full-length and residue-58 human HLCS isoforms expressed in E. coli limitations: Minimal-substrate kinetics do not prove a universal tissue allocation hierarchy; expression host is not the protein species. exposure: Biotin/ATP activation and single-turnover biotin transfer evidence_span: {"source_cache": "artifacts/biotin-research/19740736.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d785655901465bc9798378986d954b87111e3bd73d6877d9d60ae3d95cac0a37", "start_char": 2587, "end_char": 3080, "text_sha256": "fa0ec838311a45e8ccebf38a73e340a46417eae6bc300064c1165a4a0b711889"} [b7-p19740736] Distinct amino termini of two human HCS isoforms influence biotin acceptor substrate recognition. (2009). https://pubmed.ncbi.nlm.nih.gov/19740736/ DOI: 10.1074/jbc.m109.046201
Complete structured claim and evidence
Biotinidase releases biotin from its linkage to the epsilon-amino group of lysine, allowing the cofactor to be reused.
Human biotinidase / BTD → Biocytin / N-epsilon-biotinyl-L-lysine source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/6883721.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f881dd651d45537377661fc515239c3babb7160c3dbd53b8b0611ba33625aaa", "start_char": 0, "end_char": 1500, "text_sha256": "0f881dd651d45537377661fc515239c3babb7160c3dbd53b8b0611ba33625aaa"}
experimental_model
Serum enzyme assays in 5 children with late-onset multiple carboxylase deficiency and family members
exposure
Inherited deficiency; patient/control comparison
limitations
Early small case series; the serum enzyme phenotype is genetic machinery impairment, not proof of low dietary intake.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Biotinidase recovers biotin after biotin-containing material is broken down.
primary_references
[b7-p6883721] Biotinidase deficiency: the enzymatic defect in late-onset multiple carboxylase deficiency. (1983). https://pubmed.ncbi.nlm.nih.gov/6883721/ DOI: 10.1016/0009-8981(83)90096-7
tissue_or_cell_type
Serum and biochemical disease phenotype
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 455–466
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Serum enzyme assays in 5 children with late-onset multiple carboxylase deficiency and family members · source_derived_draft · unverified_draft
### b7-btd-recycling Biotinidase releases biotin from its linkage to the epsilon-amino group of lysine, allowing the cofactor to be reused. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Biotinidase recovers biotin after biotin-containing material is broken down. organism: Homo sapiens tissue_or_cell_type: Serum and biochemical disease phenotype experimental_model: Serum enzyme assays in 5 children with late-onset multiple carboxylase deficiency and family members limitations: Early small case series; the serum enzyme phenotype is genetic machinery impairment, not proof of low dietary intake. exposure: Inherited deficiency; patient/control comparison evidence_span: {"source_cache": "artifacts/biotin-research/6883721.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f881dd651d45537377661fc515239c3babb7160c3dbd53b8b0611ba33625aaa", "start_char": 0, "end_char": 1500, "text_sha256": "0f881dd651d45537377661fc515239c3babb7160c3dbd53b8b0611ba33625aaa"} [b7-p6883721] Biotinidase deficiency: the enzymatic defect in late-onset multiple carboxylase deficiency. (1983). https://pubmed.ncbi.nlm.nih.gov/6883721/ DOI: 10.1016/0009-8981(83)90096-7
Complete structured claim and evidence
Human PC catalyzes two-step pyruvate carboxylation to oxaloacetate.
Human pyruvate carboxylase / PC → Pyruvate source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/36283412.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2a5fb8ec1c27e243b8c8ba158f2c58ab1592d9895eecf16438175b2a5778de15", "start_char": 0, "end_char": 1060, "text_sha256": "2a5fb8ec1c27e243b8c8ba158f2c58ab1592d9895eecf16438175b2a5778de15"}
experimental_model
Time-resolved cryo-EM and biochemical analysis of human PC
exposure
Pyruvate, ATP and acetyl-CoA catalytic conditions
limitations
Purified-enzyme regulation is not evidence that consuming B5 or biotin stimulates this pathway in every tissue.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
PC replenishes a key carbon molecule used by several metabolic pathways.
primary_references
[b7-p36283412] Mechanistic insight into allosteric activation of human pyruvate carboxylase by acetyl-CoA. (2022). https://pubmed.ncbi.nlm.nih.gov/36283412/ DOI: 10.1016/j.molcel.2022.09.033
tissue_or_cell_type
Purified human pyruvate carboxylase
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 546–557
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-resolved cryo-EM and biochemical analysis of human PC · source_derived_draft · unverified_draft
### b7-pc-reaction Human PC catalyzes two-step pyruvate carboxylation to oxaloacetate. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: PC replenishes a key carbon molecule used by several metabolic pathways. organism: Homo sapiens tissue_or_cell_type: Purified human pyruvate carboxylase experimental_model: Time-resolved cryo-EM and biochemical analysis of human PC limitations: Purified-enzyme regulation is not evidence that consuming B5 or biotin stimulates this pathway in every tissue. exposure: Pyruvate, ATP and acetyl-CoA catalytic conditions evidence_span: {"source_cache": "artifacts/biotin-research/36283412.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2a5fb8ec1c27e243b8c8ba158f2c58ab1592d9895eecf16438175b2a5778de15", "start_char": 0, "end_char": 1060, "text_sha256": "2a5fb8ec1c27e243b8c8ba158f2c58ab1592d9895eecf16438175b2a5778de15"} [b7-p36283412] Mechanistic insight into allosteric activation of human pyruvate carboxylase by acetyl-CoA. (2022). https://pubmed.ncbi.nlm.nih.gov/36283412/ DOI: 10.1016/j.molcel.2022.09.033
Complete structured claim and evidence
Human PCC supplies (S)-methylmalonyl-CoA by propionyl-CoA carboxylation upstream of the MCEE-MMUT sequence examined in fibroblast assays.
Human propionyl-CoA carboxylase / PCC → Propionyl-CoA source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
evidence_location
Indexed primary abstract; Full text Methods 2.6 and Results 3.6; Figure 5
experimental_model
Human fibroblast PCC and coupled-pathway assays
exposure
Propionyl-CoA, ATP and bicarbonate in enzyme pathway
limitations
Pathway assignment combines human PCC characterization with coupled assays; it is not a simultaneous dietary biotin/B12 intervention.
nutrient_topic
Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
organism
Homo sapiens
plain_language
Biotin-dependent PCC makes the precursor that must be rearranged before human MMUT can use B12 on it.
primary_references
[hsia-1979-pcc] Human propionyl CoA carboxylase: some properties of the partially purified enzyme in fibroblasts from controls and patients with propionic acidemia. (1979). https://pubmed.ncbi.nlm.nih.gov/481943/ DOI: 10.1203/00006450-197906000-00005 [heuberger-2019-mcee] Genetic, structural, and functional analysis of pathogenic variations causing methylmalonyl-CoA epimerase deficiency. (2019). https://pubmed.ncbi.nlm.nih.gov/30682498/ DOI: 10.1016/j.bbadis.2019.01.021
tissue_or_cell_type
Fibroblasts
Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1159–1172
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human fibroblast PCC and coupled-pathway assays · source_derived_draft · unverified_draft
### pcc-carboxylation-upstream-b12 Human PCC supplies (S)-methylmalonyl-CoA by propionyl-CoA carboxylation upstream of the MCEE-MMUT sequence examined in fibroblast assays. Condition category: normal nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Biotin-dependent PCC makes the precursor that must be rearranged before human MMUT can use B12 on it. organism: Homo sapiens tissue_or_cell_type: Fibroblasts experimental_model: Human fibroblast PCC and coupled-pathway assays limitations: Pathway assignment combines human PCC characterization with coupled assays; it is not a simultaneous dietary biotin/B12 intervention. exposure: Propionyl-CoA, ATP and bicarbonate in enzyme pathway cross_nutrient: true evidence_location: Indexed primary abstract; Full text Methods 2.6 and Results 3.6; Figure 5 [hsia-1979-pcc] Human propionyl CoA carboxylase: some properties of the partially purified enzyme in fibroblasts from controls and patients with propionic acidemia. (1979). https://pubmed.ncbi.nlm.nih.gov/481943/ DOI: 10.1203/00006450-197906000-00005 [heuberger-2019-mcee] Genetic, structural, and functional analysis of pathogenic variations causing methylmalonyl-CoA epimerase deficiency. (2019). https://pubmed.ncbi.nlm.nih.gov/30682498/ DOI: 10.1016/j.bbadis.2019.01.021
Complete structured claim and evidence
Human MCEE interconverts methylmalonyl-CoA epimers, supplying the (R) form for MMUT; MCEE expression increased coupled succinate production.
Human methylmalonyl-CoA epimerase / MCEE → (S)-Methylmalonyl-CoA source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Full text Methods 2.6 and Results 3.6; Figure 5
experimental_model
Human fibroblast lysates overexpressing MCEE and/or MMUT
exposure
Radiolabeled propionyl-CoA; MCEE/MMUT expression and AdoCbl
limitations
Coupled labeled hydrolysis-product assay; MCEE being limiting here is not a universal in-vivo rate limitation.
nutrient_topic
Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
organism
Homo sapiens
plain_language
Human fibroblast assays showed why the epimerase step matters before the B12 enzyme.
primary_references
[heuberger-2019-mcee] Genetic, structural, and functional analysis of pathogenic variations causing methylmalonyl-CoA epimerase deficiency. (2019). https://pubmed.ncbi.nlm.nih.gov/30682498/ DOI: 10.1016/j.bbadis.2019.01.021
tissue_or_cell_type
Fibroblasts
Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1174–1186
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human fibroblast lysates overexpressing MCEE and/or MMUT · source_derived_draft · unverified_draft
### mcee-epimerizes-methylmalonyl-coa Human MCEE interconverts methylmalonyl-CoA epimers, supplying the (R) form for MMUT; MCEE expression increased coupled succinate production. Condition category: normal nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Human fibroblast assays showed why the epimerase step matters before the B12 enzyme. organism: Homo sapiens tissue_or_cell_type: Fibroblasts experimental_model: Human fibroblast lysates overexpressing MCEE and/or MMUT limitations: Coupled labeled hydrolysis-product assay; MCEE being limiting here is not a universal in-vivo rate limitation. exposure: Radiolabeled propionyl-CoA; MCEE/MMUT expression and AdoCbl cross_nutrient: false evidence_location: Full text Methods 2.6 and Results 3.6; Figure 5 [heuberger-2019-mcee] Genetic, structural, and functional analysis of pathogenic variations causing methylmalonyl-CoA epimerase deficiency. (2019). https://pubmed.ncbi.nlm.nih.gov/30682498/ DOI: 10.1016/j.bbadis.2019.01.021
Complete structured claim and evidence
Adenosylcobalamin-loaded human MMUT converts (R)-methylmalonyl-CoA to succinyl-CoA in the coupled enzyme assay.
Human methylmalonyl-CoA mutase / MMUT → (R)-Methylmalonyl-CoA source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Full text Results; Figures 2-4; cofactor off-loading and MMUT activity Methods
experimental_model
Purified human proteins
exposure
AdoCbl-loaded MMUT and methylmalonyl-CoA; thiokinase-coupled readout
limitations
Product formation is a coupled assay; cellular net flux was not measured.
nutrient_topic
Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
organism
Homo sapiens
plain_language
Purified human MMUT used activated B12 to make succinyl-CoA from the matching methylmalonyl-CoA epimer.
primary_references
[mascarenhas-2023-nanoassembly] Architecture of the human G-protein-methylmalonyl-CoA mutase nanoassembly for B12 delivery and repair. (2023). https://pubmed.ncbi.nlm.nih.gov/37468522/ DOI: 10.1038/s41467-023-40077-4
tissue_or_cell_type
Purified protein assay
Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1103–1115
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human proteins · source_derived_draft · unverified_draft
### mmut-isomerizes-r-methylmalonyl-coa Adenosylcobalamin-loaded human MMUT converts (R)-methylmalonyl-CoA to succinyl-CoA in the coupled enzyme assay. Condition category: normal nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Purified human MMUT used activated B12 to make succinyl-CoA from the matching methylmalonyl-CoA epimer. organism: Homo sapiens tissue_or_cell_type: Purified protein assay experimental_model: Purified human proteins limitations: Product formation is a coupled assay; cellular net flux was not measured. exposure: AdoCbl-loaded MMUT and methylmalonyl-CoA; thiokinase-coupled readout cross_nutrient: false evidence_location: Full text Results; Figures 2-4; cofactor off-loading and MMUT activity Methods [mascarenhas-2023-nanoassembly] Architecture of the human G-protein-methylmalonyl-CoA mutase nanoassembly for B12 delivery and repair. (2023). https://pubmed.ncbi.nlm.nih.gov/37468522/ DOI: 10.1038/s41467-023-40077-4
Complete structured claim and evidence
MCC converts 3-methylcrotonyl-CoA to 3-methylglutaconyl-CoA in the leucine breakdown pathway using biotin.
Human 3-methylcrotonyl-CoA carboxylase complex → 3-Methylcrotonyl-CoA source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/21918059.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5cf1d7e25ae7bdfeb2ac3225cee8e4e660723d5197fc057f63327b3ad9eb3aaf", "start_char": 0, "end_char": 1723, "text_sha256": "5cf1d7e25ae7bdfeb2ac3225cee8e4e660723d5197fc057f63327b3ad9eb3aaf"}
experimental_model
Two human egg-white biotin-depletion cohorts with leucine challenges
exposure
28-day depletion in cohorts of 5 and 7 adults
limitations
Biomarker challenge study; the core MCC reaction is pathway background, not a new structural discovery.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Biotin helps process a carbon intermediate produced while breaking down leucine.
primary_references
[b7-p21918059] Urinary excretion of 3-hydroxyisovaleric acid and 3-hydroxyisovaleryl carnitine increases in response to a leucine challenge in marginally biotin-deficient humans. (2011). https://pubmed.ncbi.nlm.nih.gov/21918059/ DOI: 10.3945/jn.111.146126
tissue_or_cell_type
Leucine metabolism and urine
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 793–804
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two human egg-white biotin-depletion cohorts with leucine challenges · source_derived_draft · unverified_draft
### b7-mcc-reaction MCC converts 3-methylcrotonyl-CoA to 3-methylglutaconyl-CoA in the leucine breakdown pathway using biotin. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Biotin helps process a carbon intermediate produced while breaking down leucine. organism: Homo sapiens tissue_or_cell_type: Leucine metabolism and urine experimental_model: Two human egg-white biotin-depletion cohorts with leucine challenges limitations: Biomarker challenge study; the core MCC reaction is pathway background, not a new structural discovery. exposure: 28-day depletion in cohorts of 5 and 7 adults evidence_span: {"source_cache": "artifacts/biotin-research/21918059.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5cf1d7e25ae7bdfeb2ac3225cee8e4e660723d5197fc057f63327b3ad9eb3aaf", "start_char": 0, "end_char": 1723, "text_sha256": "5cf1d7e25ae7bdfeb2ac3225cee8e4e660723d5197fc057f63327b3ad9eb3aaf"} [b7-p21918059] Urinary excretion of 3-hydroxyisovaleric acid and 3-hydroxyisovaleryl carnitine increases in response to a leucine challenge in marginally biotin-deficient humans. (2011). https://pubmed.ncbi.nlm.nih.gov/21918059/ DOI: 10.3945/jn.111.146126
Complete structured claim and evidence
Human ACC1 uses biotin-dependent carboxylation of acetyl-CoA to generate malonyl-CoA.
Human acetyl-CoA carboxylase 1 / ACACA → Acetyl-CoA source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/39383219.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5f7d3cd6a5865a03b8dc9c510f60249ee2c9f6516773780e5d7b4aef0a9b2db8", "start_char": 0, "end_char": 309, "text_sha256": "b094342ce091c8f919d065311ecd04ddd0c6b9b2824ba8adedd5768424a81a71"}
experimental_model
Cryo-EM of endogenous and recombinant human ACC1 filaments
exposure
Inactive substrate-containing and dephosphorylated/citrate-treated states
limitations
Filament presence alone does not mean enzyme activation; the paper resolved both active and inactive arrangements.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
ACC1 makes a building block used in fatty-acid synthesis.
primary_references
[b7-p39383219] Filament structures unveil the dynamic organization of human acetyl-CoA carboxylase. (2024). https://pubmed.ncbi.nlm.nih.gov/39383219/ DOI: 10.1126/sciadv.ado4880
tissue_or_cell_type
Purified human ACC1
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 637–648
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of endogenous and recombinant human ACC1 filaments · source_derived_draft · unverified_draft
### b7-acc1-reaction Human ACC1 uses biotin-dependent carboxylation of acetyl-CoA to generate malonyl-CoA. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: ACC1 makes a building block used in fatty-acid synthesis. organism: Homo sapiens tissue_or_cell_type: Purified human ACC1 experimental_model: Cryo-EM of endogenous and recombinant human ACC1 filaments limitations: Filament presence alone does not mean enzyme activation; the paper resolved both active and inactive arrangements. exposure: Inactive substrate-containing and dephosphorylated/citrate-treated states evidence_span: {"source_cache": "artifacts/biotin-research/39383219.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5f7d3cd6a5865a03b8dc9c510f60249ee2c9f6516773780e5d7b4aef0a9b2db8", "start_char": 0, "end_char": 309, "text_sha256": "b094342ce091c8f919d065311ecd04ddd0c6b9b2824ba8adedd5768424a81a71"} [b7-p39383219] Filament structures unveil the dynamic organization of human acetyl-CoA carboxylase. (2024). https://pubmed.ncbi.nlm.nih.gov/39383219/ DOI: 10.1126/sciadv.ado4880
Complete structured claim and evidence
Purified human ACC2 formed malonyl-CoA from acetyl-CoA in assays varying bicarbonate and ATP.
Human acetyl-CoA carboxylase 2 / ACACB → Acetyl-CoA source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/19236960.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bedd791235b10ff5942ef7177b54bca5b2243883da02fb24572691aaf5975be5", "start_char": 0, "end_char": 896, "text_sha256": "bedd791235b10ff5942ef7177b54bca5b2243883da02fb24572691aaf5975be5"}
experimental_model
Steady-state kinetics of purified recombinant human ACC2; LC-MS/MS malonyl-CoA assay
exposure
Bicarbonate, ATP, acetyl-CoA and citrate concentration matrices
limitations
Kinetic constants are assay properties; they do not define a dietary biotin or B5 threshold.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
ACC2 makes the same carbon product as ACC1 but serves a distinct enzyme context.
primary_references
[b7-p19236960] Characterization of recombinant human acetyl-CoA carboxylase-2 steady-state kinetics. (2009). https://pubmed.ncbi.nlm.nih.gov/19236960/ DOI: 10.1016/j.bbapap.2009.02.004
tissue_or_cell_type
Purified human ACC2
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 676–687
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Steady-state kinetics of purified recombinant human ACC2; LC-MS/MS malonyl-CoA assay · source_derived_draft · unverified_draft
### b7-acc2-reaction Purified human ACC2 formed malonyl-CoA from acetyl-CoA in assays varying bicarbonate and ATP. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: ACC2 makes the same carbon product as ACC1 but serves a distinct enzyme context. organism: Homo sapiens tissue_or_cell_type: Purified human ACC2 experimental_model: Steady-state kinetics of purified recombinant human ACC2; LC-MS/MS malonyl-CoA assay limitations: Kinetic constants are assay properties; they do not define a dietary biotin or B5 threshold. exposure: Bicarbonate, ATP, acetyl-CoA and citrate concentration matrices evidence_span: {"source_cache": "artifacts/biotin-research/19236960.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bedd791235b10ff5942ef7177b54bca5b2243883da02fb24572691aaf5975be5", "start_char": 0, "end_char": 896, "text_sha256": "bedd791235b10ff5942ef7177b54bca5b2243883da02fb24572691aaf5975be5"} [b7-p19236960] Characterization of recombinant human acetyl-CoA carboxylase-2 steady-state kinetics. (2009). https://pubmed.ncbi.nlm.nih.gov/19236960/ DOI: 10.1016/j.bbapap.2009.02.004
Complete structured claim and evidence
Acetyl-CoA stabilized human PC in a catalytically competent conformation in time-resolved structural and biochemical experiments.
Acetyl-CoA → Human pyruvate carboxylase / PC source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/36283412.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2a5fb8ec1c27e243b8c8ba158f2c58ab1592d9895eecf16438175b2a5778de15", "start_char": 0, "end_char": 1060, "text_sha256": "2a5fb8ec1c27e243b8c8ba158f2c58ab1592d9895eecf16438175b2a5778de15"}
experimental_model
Time-resolved cryo-EM and biochemical analysis of human PC
exposure
Pyruvate, ATP and acetyl-CoA catalytic conditions
limitations
Purified-enzyme regulation is not evidence that consuming B5 or biotin stimulates this pathway in every tissue.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Acetyl-CoA helps put PC into its working shape.
primary_references
[b7-p36283412] Mechanistic insight into allosteric activation of human pyruvate carboxylase by acetyl-CoA. (2022). https://pubmed.ncbi.nlm.nih.gov/36283412/ DOI: 10.1016/j.molcel.2022.09.033
tissue_or_cell_type
Purified human pyruvate carboxylase
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 559–570
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-resolved cryo-EM and biochemical analysis of human PC · source_derived_draft · unverified_draft
### b7-pc-acetylcoa Acetyl-CoA stabilized human PC in a catalytically competent conformation in time-resolved structural and biochemical experiments. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Acetyl-CoA helps put PC into its working shape. organism: Homo sapiens tissue_or_cell_type: Purified human pyruvate carboxylase experimental_model: Time-resolved cryo-EM and biochemical analysis of human PC limitations: Purified-enzyme regulation is not evidence that consuming B5 or biotin stimulates this pathway in every tissue. exposure: Pyruvate, ATP and acetyl-CoA catalytic conditions evidence_span: {"source_cache": "artifacts/biotin-research/36283412.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2a5fb8ec1c27e243b8c8ba158f2c58ab1592d9895eecf16438175b2a5778de15", "start_char": 0, "end_char": 1060, "text_sha256": "2a5fb8ec1c27e243b8c8ba158f2c58ab1592d9895eecf16438175b2a5778de15"} [b7-p36283412] Mechanistic insight into allosteric activation of human pyruvate carboxylase by acetyl-CoA. (2022). https://pubmed.ncbi.nlm.nih.gov/36283412/ DOI: 10.1016/j.molcel.2022.09.033
Complete structured claim and evidence
Wild-type human CPT1B showed high-affinity malonyl-CoA binding and inhibition in recombinant mitochondrial assays.
Malonyl-CoA → Human carnitine palmitoyltransferase 1B / CPT1B source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/10651636.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e99728ef83700f17a810421385b71ea243576419df807dc4749b588beb01d400", "start_char": 0, "end_char": 1542, "text_sha256": "e99728ef83700f17a810421385b71ea243576419df807dc4749b588beb01d400"}
experimental_model
Human CPT1B wild type and N-terminal deletions expressed in yeast mitochondria
exposure
Malonyl-CoA binding and activity assays
limitations
Expression host is yeast; these data concern human CPT1B, not every CPT1 isoform or a biotin supplementation outcome.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Malonyl-CoA links the carboxylase pathway to the carnitine-dependent fat-entry step.
primary_references
[b7-p10651636] The first 28 N-terminal amino acid residues of human heart muscle carnitine palmitoyltransferase I are essential for malonyl CoA sensitivity and high-affinity binding. (2000). https://pubmed.ncbi.nlm.nih.gov/10651636/ DOI: 10.1021/bi9918700
tissue_or_cell_type
Recombinant human muscle/heart CPT1B
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 741–752
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CPT1B wild type and N-terminal deletions expressed in yeast mitochondria · source_derived_draft · unverified_draft
### b7-malonyl-cpt1b Wild-type human CPT1B showed high-affinity malonyl-CoA binding and inhibition in recombinant mitochondrial assays. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Malonyl-CoA links the carboxylase pathway to the carnitine-dependent fat-entry step. organism: Homo sapiens tissue_or_cell_type: Recombinant human muscle/heart CPT1B experimental_model: Human CPT1B wild type and N-terminal deletions expressed in yeast mitochondria limitations: Expression host is yeast; these data concern human CPT1B, not every CPT1 isoform or a biotin supplementation outcome. exposure: Malonyl-CoA binding and activity assays evidence_span: {"source_cache": "artifacts/biotin-research/10651636.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e99728ef83700f17a810421385b71ea243576419df807dc4749b588beb01d400", "start_char": 0, "end_char": 1542, "text_sha256": "e99728ef83700f17a810421385b71ea243576419df807dc4749b588beb01d400"} [b7-p10651636] The first 28 N-terminal amino acid residues of human heart muscle carnitine palmitoyltransferase I are essential for malonyl CoA sensitivity and high-affinity binding. (2000). https://pubmed.ncbi.nlm.nih.gov/10651636/ DOI: 10.1021/bi9918700
Complete structured claim and evidence
Biotin uptake in human NCM460 cells was saturable, energy dependent and sodium dependent, with apparent Km 19.7 micromolar.
Biotin → Human colonic epithelial biotin uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"}
experimental_model
Transport and inhibitor experiments in human NCM460 colonic epithelial cells
exposure
Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators
limitations
Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Colon cells can take up free biotin through a saturable transport process.
primary_references
[b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365
tissue_or_cell_type
Colonic epithelium; NCM460 culture
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 182–193
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transport and inhibitor experiments in human NCM460 colonic epithelial cells · source_derived_draft · unverified_draft
### b7-colon-sodium Biotin uptake in human NCM460 cells was saturable, energy dependent and sodium dependent, with apparent Km 19.7 micromolar. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Colon cells can take up free biotin through a saturable transport process. organism: Homo sapiens tissue_or_cell_type: Colonic epithelium; NCM460 culture experimental_model: Transport and inhibitor experiments in human NCM460 colonic epithelial cells limitations: Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes. exposure: Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators evidence_span: {"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"} [b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365
Complete structured claim and evidence
Pantothenic acid competitively inhibited biotin uptake in NCM460 cells, with Ki 14.4 micromolar.
Pantothenate (vitamin B5) → Human colonic epithelial biotin uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"}
experimental_model
Transport and inhibitor experiments in human NCM460 colonic epithelial cells
exposure
Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators
limitations
Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
B5 and biotin can compete for entry in this colon-cell assay.
primary_references
[b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365
tissue_or_cell_type
Colonic epithelium; NCM460 culture
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 195–206
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transport and inhibitor experiments in human NCM460 colonic epithelial cells · source_derived_draft · unverified_draft
### b7-colon-b5-competition Pantothenic acid competitively inhibited biotin uptake in NCM460 cells, with Ki 14.4 micromolar. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: B5 and biotin can compete for entry in this colon-cell assay. organism: Homo sapiens tissue_or_cell_type: Colonic epithelium; NCM460 culture experimental_model: Transport and inhibitor experiments in human NCM460 colonic epithelial cells limitations: Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes. exposure: Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators evidence_span: {"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"} [b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365
Complete structured claim and evidence
PKC activators reduced biotin uptake in NCM460 cells; PKC inhibitors modestly increased uptake.
Protein kinase C family → Human colonic epithelial biotin uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"}
experimental_model
Transport and inhibitor experiments in human NCM460 colonic epithelial cells
exposure
Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators
limitations
Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Cell signaling changes how quickly colon cells admit biotin.
primary_references
[b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365
tissue_or_cell_type
Colonic epithelium; NCM460 culture
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 208–219
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transport and inhibitor experiments in human NCM460 colonic epithelial cells · source_derived_draft · unverified_draft
### b7-colon-pkc PKC activators reduced biotin uptake in NCM460 cells; PKC inhibitors modestly increased uptake. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cell signaling changes how quickly colon cells admit biotin. organism: Homo sapiens tissue_or_cell_type: Colonic epithelium; NCM460 culture experimental_model: Transport and inhibitor experiments in human NCM460 colonic epithelial cells limitations: Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes. exposure: Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators evidence_span: {"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"} [b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365
Complete structured claim and evidence
Chronic ethanol exposure reduced activity of both SLC5A6 promoters P1 and P2 in human Caco-2 cells.
Ethanol → Human intestinal SLC5A6 promoter activity source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/21148397.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2398f4926e678d4650eba6488cab945c2d651a7c8e6c2f8fd00794c0ea891d4d", "start_char": 0, "end_char": 1829, "text_sha256": "2398f4926e678d4650eba6488cab945c2d651a7c8e6c2f8fd00794c0ea891d4d"}
experimental_model
Chronic ethanol exposure in rodents and human Caco-2 cells
exposure
Chronic ethanol feeding or culture exposure
limitations
Animal feeding and human cell experiments are separate; no human dietary depletion threshold was established.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Alcohol exposure reduced the cell signals that produce the shared vitamin transporter.
primary_references
[b7-p21148397] Inhibition of intestinal biotin absorption by chronic alcohol feeding: cellular and molecular mechanisms. (2011). https://pubmed.ncbi.nlm.nih.gov/21148397/ DOI: 10.1152/ajpgi.00465.2010
tissue_or_cell_type
Caco-2 intestinal epithelial cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 221–232
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chronic ethanol exposure in rodents and human Caco-2 cells · source_derived_draft · unverified_draft
### b7-alcohol-promoters Chronic ethanol exposure reduced activity of both SLC5A6 promoters P1 and P2 in human Caco-2 cells. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Alcohol exposure reduced the cell signals that produce the shared vitamin transporter. organism: Homo sapiens tissue_or_cell_type: Caco-2 intestinal epithelial cells experimental_model: Chronic ethanol exposure in rodents and human Caco-2 cells limitations: Animal feeding and human cell experiments are separate; no human dietary depletion threshold was established. exposure: Chronic ethanol feeding or culture exposure evidence_span: {"source_cache": "artifacts/biotin-research/21148397.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2398f4926e678d4650eba6488cab945c2d651a7c8e6c2f8fd00794c0ea891d4d", "start_char": 0, "end_char": 1829, "text_sha256": "2398f4926e678d4650eba6488cab945c2d651a7c8e6c2f8fd00794c0ea891d4d"} [b7-p21148397] Inhibition of intestinal biotin absorption by chronic alcohol feeding: cellular and molecular mechanisms. (2011). https://pubmed.ncbi.nlm.nih.gov/21148397/ DOI: 10.1152/ajpgi.00465.2010
Complete structured claim and evidence
Chronic ethanol feeding reduced carrier-mediated biotin uptake across rat jejunal brush-border and basolateral membranes.
Ethanol → Rat intestinal biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/21148397.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2398f4926e678d4650eba6488cab945c2d651a7c8e6c2f8fd00794c0ea891d4d", "start_char": 0, "end_char": 1829, "text_sha256": "2398f4926e678d4650eba6488cab945c2d651a7c8e6c2f8fd00794c0ea891d4d"}
experimental_model
Chronic ethanol exposure in rodents and human Caco-2 cells
exposure
Chronic ethanol feeding or culture exposure
limitations
Animal feeding and human cell experiments are separate; no human dietary depletion threshold was established.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Rattus norvegicus
plain_language
In rats, chronic alcohol feeding impaired both measured sides of intestinal biotin transport.
primary_references
[b7-p21148397] Inhibition of intestinal biotin absorption by chronic alcohol feeding: cellular and molecular mechanisms. (2011). https://pubmed.ncbi.nlm.nih.gov/21148397/ DOI: 10.1152/ajpgi.00465.2010
tissue_or_cell_type
Rat jejunal membrane preparations
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 234–245
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chronic ethanol exposure in rodents and human Caco-2 cells · source_derived_draft · unverified_draft
### b7-alcohol-rat-uptake Chronic ethanol feeding reduced carrier-mediated biotin uptake across rat jejunal brush-border and basolateral membranes. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: In rats, chronic alcohol feeding impaired both measured sides of intestinal biotin transport. organism: Rattus norvegicus tissue_or_cell_type: Rat jejunal membrane preparations experimental_model: Chronic ethanol exposure in rodents and human Caco-2 cells limitations: Animal feeding and human cell experiments are separate; no human dietary depletion threshold was established. exposure: Chronic ethanol feeding or culture exposure evidence_span: {"source_cache": "artifacts/biotin-research/21148397.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2398f4926e678d4650eba6488cab945c2d651a7c8e6c2f8fd00794c0ea891d4d", "start_char": 0, "end_char": 1829, "text_sha256": "2398f4926e678d4650eba6488cab945c2d651a7c8e6c2f8fd00794c0ea891d4d"} [b7-p21148397] Inhibition of intestinal biotin absorption by chronic alcohol feeding: cellular and molecular mechanisms. (2011). https://pubmed.ncbi.nlm.nih.gov/21148397/ DOI: 10.1152/ajpgi.00465.2010
Complete structured claim and evidence
Chronic ethanol exposure reduced carrier-mediated biotin uptake in human HK-2 cells.
Ethanol → Human renal proximal-tubular biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/21209005.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b42defcb27acffce0c264240e14b0535770f94627ee5a4836b284e4e0971b5a0", "start_char": 0, "end_char": 1797, "text_sha256": "b42defcb27acffce0c264240e14b0535770f94627ee5a4836b284e4e0971b5a0"}
experimental_model
Chronic ethanol exposure in renal HK-2 cells and separate rodents
exposure
Chronic ethanol exposure
limitations
HK-2 uptake is a model of renal handling, not a measured whole-body biotin loss in people.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Kidney cells reclaimed less biotin in this alcohol-exposure model.
primary_references
[b7-p21209005] Chronic alcohol exposure negatively impacts the physiological and molecular parameters of the renal biotin reabsorption process. (2011). https://pubmed.ncbi.nlm.nih.gov/21209005/ DOI: 10.1152/ajprenal.00707.2010
tissue_or_cell_type
Human HK-2 proximal-tubular epithelial cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 247–258
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chronic ethanol exposure in renal HK-2 cells and separate rodents · source_derived_draft · unverified_draft
### b7-kidney-alcohol-uptake Chronic ethanol exposure reduced carrier-mediated biotin uptake in human HK-2 cells. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Kidney cells reclaimed less biotin in this alcohol-exposure model. organism: Homo sapiens tissue_or_cell_type: Human HK-2 proximal-tubular epithelial cells experimental_model: Chronic ethanol exposure in renal HK-2 cells and separate rodents limitations: HK-2 uptake is a model of renal handling, not a measured whole-body biotin loss in people. exposure: Chronic ethanol exposure evidence_span: {"source_cache": "artifacts/biotin-research/21209005.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b42defcb27acffce0c264240e14b0535770f94627ee5a4836b284e4e0971b5a0", "start_char": 0, "end_char": 1797, "text_sha256": "b42defcb27acffce0c264240e14b0535770f94627ee5a4836b284e4e0971b5a0"} [b7-p21209005] Chronic alcohol exposure negatively impacts the physiological and molecular parameters of the renal biotin reabsorption process. (2011). https://pubmed.ncbi.nlm.nih.gov/21209005/ DOI: 10.1152/ajprenal.00707.2010
Complete structured claim and evidence
Ethanol-exposed HK-2 cells showed reduced activity of the human SLC5A6 regulatory region.
Ethanol → Human renal SLC5A6 promoter activity source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/21209005.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b42defcb27acffce0c264240e14b0535770f94627ee5a4836b284e4e0971b5a0", "start_char": 0, "end_char": 1797, "text_sha256": "b42defcb27acffce0c264240e14b0535770f94627ee5a4836b284e4e0971b5a0"}
experimental_model
Chronic ethanol exposure in renal HK-2 cells and separate rodents
exposure
Chronic ethanol exposure
limitations
HK-2 uptake is a model of renal handling, not a measured whole-body biotin loss in people.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Reduced transporter production is one explanation for the impaired uptake.
primary_references
[b7-p21209005] Chronic alcohol exposure negatively impacts the physiological and molecular parameters of the renal biotin reabsorption process. (2011). https://pubmed.ncbi.nlm.nih.gov/21209005/ DOI: 10.1152/ajprenal.00707.2010
tissue_or_cell_type
Human HK-2 proximal-tubular epithelial cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 260–271
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chronic ethanol exposure in renal HK-2 cells and separate rodents · source_derived_draft · unverified_draft
### b7-kidney-alcohol-transcription Ethanol-exposed HK-2 cells showed reduced activity of the human SLC5A6 regulatory region. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reduced transporter production is one explanation for the impaired uptake. organism: Homo sapiens tissue_or_cell_type: Human HK-2 proximal-tubular epithelial cells experimental_model: Chronic ethanol exposure in renal HK-2 cells and separate rodents limitations: HK-2 uptake is a model of renal handling, not a measured whole-body biotin loss in people. exposure: Chronic ethanol exposure evidence_span: {"source_cache": "artifacts/biotin-research/21209005.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b42defcb27acffce0c264240e14b0535770f94627ee5a4836b284e4e0971b5a0", "start_char": 0, "end_char": 1797, "text_sha256": "b42defcb27acffce0c264240e14b0535770f94627ee5a4836b284e4e0971b5a0"} [b7-p21209005] Chronic alcohol exposure negatively impacts the physiological and molecular parameters of the renal biotin reabsorption process. (2011). https://pubmed.ncbi.nlm.nih.gov/21209005/ DOI: 10.1152/ajprenal.00707.2010
Complete structured claim and evidence
Carbamazepine competitively inhibited biotin uptake in human intestinal brush-border vesicles (Ki 4.70 mmol/L), without inhibiting basolateral biotin transport.
Carbamazepine → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/2911998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb", "start_char": 0, "end_char": 1045, "text_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb"}
experimental_model
Transport assays in purified human intestinal brush-border and basolateral membrane vesicles
exposure
Carbamazepine or primidone; millimolar inhibitor constants
limitations
These are membrane-assay concentrations. The study does not establish that prescribed doses cause deficiency in every patient.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
The drug competed with biotin at the gut-facing membrane in this experiment.
primary_references
[b7-p2911998] Biotin transport in the human intestine: inhibition by anticonvulsant drugs. (1989). https://pubmed.ncbi.nlm.nih.gov/2911998/ DOI: 10.1093/ajcn/49.1.127
tissue_or_cell_type
Intestinal membrane vesicles
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 273–284
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transport assays in purified human intestinal brush-border and basolateral membrane vesicles · source_derived_draft · unverified_draft
### b7-carbamazepine-uptake Carbamazepine competitively inhibited biotin uptake in human intestinal brush-border vesicles (Ki 4.70 mmol/L), without inhibiting basolateral biotin transport. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The drug competed with biotin at the gut-facing membrane in this experiment. organism: Homo sapiens tissue_or_cell_type: Intestinal membrane vesicles experimental_model: Transport assays in purified human intestinal brush-border and basolateral membrane vesicles limitations: These are membrane-assay concentrations. The study does not establish that prescribed doses cause deficiency in every patient. exposure: Carbamazepine or primidone; millimolar inhibitor constants evidence_span: {"source_cache": "artifacts/biotin-research/2911998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb", "start_char": 0, "end_char": 1045, "text_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb"} [b7-p2911998] Biotin transport in the human intestine: inhibition by anticonvulsant drugs. (1989). https://pubmed.ncbi.nlm.nih.gov/2911998/ DOI: 10.1093/ajcn/49.1.127
Complete structured claim and evidence
Primidone competitively inhibited biotin uptake in human intestinal brush-border vesicles (Ki 2.25 mmol/L), without inhibiting basolateral biotin transport.
Primidone → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/2911998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb", "start_char": 0, "end_char": 1045, "text_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb"}
experimental_model
Transport assays in purified human intestinal brush-border and basolateral membrane vesicles
exposure
Carbamazepine or primidone; millimolar inhibitor constants
limitations
These are membrane-assay concentrations. The study does not establish that prescribed doses cause deficiency in every patient.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
The drug competed with biotin at the gut-facing membrane in this experiment.
primary_references
[b7-p2911998] Biotin transport in the human intestine: inhibition by anticonvulsant drugs. (1989). https://pubmed.ncbi.nlm.nih.gov/2911998/ DOI: 10.1093/ajcn/49.1.127
tissue_or_cell_type
Intestinal membrane vesicles
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 286–297
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transport assays in purified human intestinal brush-border and basolateral membrane vesicles · source_derived_draft · unverified_draft
### b7-primidone-uptake Primidone competitively inhibited biotin uptake in human intestinal brush-border vesicles (Ki 2.25 mmol/L), without inhibiting basolateral biotin transport. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The drug competed with biotin at the gut-facing membrane in this experiment. organism: Homo sapiens tissue_or_cell_type: Intestinal membrane vesicles experimental_model: Transport assays in purified human intestinal brush-border and basolateral membrane vesicles limitations: These are membrane-assay concentrations. The study does not establish that prescribed doses cause deficiency in every patient. exposure: Carbamazepine or primidone; millimolar inhibitor constants evidence_span: {"source_cache": "artifacts/biotin-research/2911998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb", "start_char": 0, "end_char": 1045, "text_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb"} [b7-p2911998] Biotin transport in the human intestine: inhibition by anticonvulsant drugs. (1989). https://pubmed.ncbi.nlm.nih.gov/2911998/ DOI: 10.1093/ajcn/49.1.127
Complete structured claim and evidence
Urinary bisnorbiotin was higher in both carbamazepine/phenytoin-treated and phenobarbital-treated children than in controls.
Carbamazepine → Human urinary bisnorbiotin excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/9523856.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136", "start_char": 0, "end_char": 1876, "text_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136"}
experimental_model
Observational urine comparison: 7 children receiving carbamazepine/phenytoin, 6 phenobarbital, 16 controls
exposure
Long-term anticonvulsant treatment
limitations
Untimed urine, small nonrandomized groups and discordant markers limit diagnosis; faster turnover is not a universal deficiency diagnosis.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Some anticonvulsant-treated children excreted more of a biotin breakdown product.
primary_references
[b7-p9523856] Disturbances in biotin metabolism in children undergoing long-term anticonvulsant therapy. (1998). https://pubmed.ncbi.nlm.nih.gov/9523856/ DOI: 10.1097/00005176-199803000-00002
tissue_or_cell_type
Urine
trigger_kind
biomarker_context Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 299–310
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Observational urine comparison: 7 children receiving carbamazepine/phenytoin, 6 phenobarbital, 16 controls · source_derived_draft · unverified_draft
### b7-drug-bisnorbiotin Urinary bisnorbiotin was higher in both carbamazepine/phenytoin-treated and phenobarbital-treated children than in controls. Condition category: biomarker_context nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some anticonvulsant-treated children excreted more of a biotin breakdown product. organism: Homo sapiens tissue_or_cell_type: Urine experimental_model: Observational urine comparison: 7 children receiving carbamazepine/phenytoin, 6 phenobarbital, 16 controls limitations: Untimed urine, small nonrandomized groups and discordant markers limit diagnosis; faster turnover is not a universal deficiency diagnosis. exposure: Long-term anticonvulsant treatment evidence_span: {"source_cache": "artifacts/biotin-research/9523856.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136", "start_char": 0, "end_char": 1876, "text_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136"} [b7-p9523856] Disturbances in biotin metabolism in children undergoing long-term anticonvulsant therapy. (1998). https://pubmed.ncbi.nlm.nih.gov/9523856/ DOI: 10.1097/00005176-199803000-00002
Complete structured claim and evidence
The carbamazepine/phenytoin group had higher urinary 3-HIA, but only one child in that group had low urinary biotin.
Carbamazepine → Human urinary 3-hydroxyisovaleric acid excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/9523856.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136", "start_char": 0, "end_char": 1876, "text_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136"}
experimental_model
Observational urine comparison: 7 children receiving carbamazepine/phenytoin, 6 phenobarbital, 16 controls
exposure
Long-term anticonvulsant treatment
limitations
Untimed urine, small nonrandomized groups and discordant markers limit diagnosis; faster turnover is not a universal deficiency diagnosis.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Different biotin-status markers did not give the same answer in these children.
primary_references
[b7-p9523856] Disturbances in biotin metabolism in children undergoing long-term anticonvulsant therapy. (1998). https://pubmed.ncbi.nlm.nih.gov/9523856/ DOI: 10.1097/00005176-199803000-00002
tissue_or_cell_type
Urine
trigger_kind
biomarker_context Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 312–323
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Observational urine comparison: 7 children receiving carbamazepine/phenytoin, 6 phenobarbital, 16 controls · source_derived_draft · unverified_draft
### b7-drug-3hia The carbamazepine/phenytoin group had higher urinary 3-HIA, but only one child in that group had low urinary biotin. Condition category: biomarker_context nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different biotin-status markers did not give the same answer in these children. organism: Homo sapiens tissue_or_cell_type: Urine experimental_model: Observational urine comparison: 7 children receiving carbamazepine/phenytoin, 6 phenobarbital, 16 controls limitations: Untimed urine, small nonrandomized groups and discordant markers limit diagnosis; faster turnover is not a universal deficiency diagnosis. exposure: Long-term anticonvulsant treatment evidence_span: {"source_cache": "artifacts/biotin-research/9523856.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136", "start_char": 0, "end_char": 1876, "text_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136"} [b7-p9523856] Disturbances in biotin metabolism in children undergoing long-term anticonvulsant therapy. (1998). https://pubmed.ncbi.nlm.nih.gov/9523856/ DOI: 10.1097/00005176-199803000-00002
Complete structured claim and evidence
Similar urinary recovery after the two larger oral biotin doses and the intravenous dose supported near-complete oral absorption in six healthy adults.
Biotin → Estimated oral biotin bioavailability in humans source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/10075337.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8eb8ff3bb786de29bfda6f596af2fe6e8fdf366d9cad84065176a825d6035ebd", "start_char": 0, "end_char": 1677, "text_sha256": "8eb8ff3bb786de29bfda6f596af2fe6e8fdf366d9cad84065176a825d6035ebd"}
experimental_model
Crossover oral and intravenous administration in 6 healthy adults
exposure
Oral 2.1, 8.2 or 81.9 micromol; intravenous 18.4 micromol biotin
limitations
Bioavailability was inferred from urinary recovery; the anomalous smallest dose and small healthy sample limit generalization to malabsorption or transporter disease.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
High oral doses were still well absorbed in this small study.
primary_references
[b7-p10075337] Bioavailability of biotin given orally to humans in pharmacologic doses. (1999). https://pubmed.ncbi.nlm.nih.gov/10075337/ DOI: 10.1093/ajcn/69.3.504
tissue_or_cell_type
Whole-body urinary recovery
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 325–336
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Crossover oral and intravenous administration in 6 healthy adults · source_derived_draft · unverified_draft
### b7-oral-bioavailability Similar urinary recovery after the two larger oral biotin doses and the intravenous dose supported near-complete oral absorption in six healthy adults. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: High oral doses were still well absorbed in this small study. organism: Homo sapiens tissue_or_cell_type: Whole-body urinary recovery experimental_model: Crossover oral and intravenous administration in 6 healthy adults limitations: Bioavailability was inferred from urinary recovery; the anomalous smallest dose and small healthy sample limit generalization to malabsorption or transporter disease. exposure: Oral 2.1, 8.2 or 81.9 micromol; intravenous 18.4 micromol biotin evidence_span: {"source_cache": "artifacts/biotin-research/10075337.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8eb8ff3bb786de29bfda6f596af2fe6e8fdf366d9cad84065176a825d6035ebd", "start_char": 0, "end_char": 1677, "text_sha256": "8eb8ff3bb786de29bfda6f596af2fe6e8fdf366d9cad84065176a825d6035ebd"} [b7-p10075337] Bioavailability of biotin given orally to humans in pharmacologic doses. (1999). https://pubmed.ncbi.nlm.nih.gov/10075337/ DOI: 10.1093/ajcn/69.3.504
Complete structured claim and evidence
Biotin represented more than half of recovered urinary biotin-related material; bisnorbiotin, sulfoxide and other metabolites contributed the remainder.
Biotin → Human urinary biotin-metabolite excretion source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/10075337.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8eb8ff3bb786de29bfda6f596af2fe6e8fdf366d9cad84065176a825d6035ebd", "start_char": 0, "end_char": 1677, "text_sha256": "8eb8ff3bb786de29bfda6f596af2fe6e8fdf366d9cad84065176a825d6035ebd"}
experimental_model
Crossover oral and intravenous administration in 6 healthy adults
exposure
Oral 2.1, 8.2 or 81.9 micromol; intravenous 18.4 micromol biotin
limitations
Bioavailability was inferred from urinary recovery; the anomalous smallest dose and small healthy sample limit generalization to malabsorption or transporter disease.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
A urine assay must distinguish intact biotin from its breakdown products.
primary_references
[b7-p10075337] Bioavailability of biotin given orally to humans in pharmacologic doses. (1999). https://pubmed.ncbi.nlm.nih.gov/10075337/ DOI: 10.1093/ajcn/69.3.504
tissue_or_cell_type
Whole-body urinary recovery
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 338–349
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Crossover oral and intravenous administration in 6 healthy adults · source_derived_draft · unverified_draft
### b7-urinary-metabolites Biotin represented more than half of recovered urinary biotin-related material; bisnorbiotin, sulfoxide and other metabolites contributed the remainder. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A urine assay must distinguish intact biotin from its breakdown products. organism: Homo sapiens tissue_or_cell_type: Whole-body urinary recovery experimental_model: Crossover oral and intravenous administration in 6 healthy adults limitations: Bioavailability was inferred from urinary recovery; the anomalous smallest dose and small healthy sample limit generalization to malabsorption or transporter disease. exposure: Oral 2.1, 8.2 or 81.9 micromol; intravenous 18.4 micromol biotin evidence_span: {"source_cache": "artifacts/biotin-research/10075337.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8eb8ff3bb786de29bfda6f596af2fe6e8fdf366d9cad84065176a825d6035ebd", "start_char": 0, "end_char": 1677, "text_sha256": "8eb8ff3bb786de29bfda6f596af2fe6e8fdf366d9cad84065176a825d6035ebd"} [b7-p10075337] Bioavailability of biotin given orally to humans in pharmacologic doses. (1999). https://pubmed.ncbi.nlm.nih.gov/10075337/ DOI: 10.1093/ajcn/69.3.504
Complete structured claim and evidence
Full-length human HLCS associated with the minimal biotin acceptor about twice as fast as the residue-58 isoform in pre-steady-state transfer measurements.
Human holocarboxylase synthetase / HLCS → Human HLCS beginning at residue 58 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/19740736.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "27724d2b900152fade1d3be186d350c2b1862e5281355990f4720236798248ed", "start_char": 0, "end_char": 1259, "text_sha256": "27724d2b900152fade1d3be186d350c2b1862e5281355990f4720236798248ed"}
experimental_model
Purified full-length and residue-58 human HLCS isoforms expressed in E. coli
exposure
Biotin/ATP activation and single-turnover biotin transfer
limitations
Minimal-substrate kinetics do not prove a universal tissue allocation hierarchy; expression host is not the protein species.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Two HLCS forms recognize an enzyme attachment site at different rates.
primary_references
[b7-p19740736] Distinct amino termini of two human HCS isoforms influence biotin acceptor substrate recognition. (2009). https://pubmed.ncbi.nlm.nih.gov/19740736/ DOI: 10.1074/jbc.m109.046201
tissue_or_cell_type
Purified proteins and minimal biotin-accepting substrate
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 377–388
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified full-length and residue-58 human HLCS isoforms expressed in E. coli · source_derived_draft · unverified_draft
### b7-hlcs-isoform-kinetics Full-length human HLCS associated with the minimal biotin acceptor about twice as fast as the residue-58 isoform in pre-steady-state transfer measurements. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Two HLCS forms recognize an enzyme attachment site at different rates. organism: Homo sapiens tissue_or_cell_type: Purified proteins and minimal biotin-accepting substrate experimental_model: Purified full-length and residue-58 human HLCS isoforms expressed in E. coli limitations: Minimal-substrate kinetics do not prove a universal tissue allocation hierarchy; expression host is not the protein species. exposure: Biotin/ATP activation and single-turnover biotin transfer evidence_span: {"source_cache": "artifacts/biotin-research/19740736.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "27724d2b900152fade1d3be186d350c2b1862e5281355990f4720236798248ed", "start_char": 0, "end_char": 1259, "text_sha256": "27724d2b900152fade1d3be186d350c2b1862e5281355990f4720236798248ed"} [b7-p19740736] Distinct amino termini of two human HCS isoforms influence biotin acceptor substrate recognition. (2009). https://pubmed.ncbi.nlm.nih.gov/19740736/ DOI: 10.1074/jbc.m109.046201
Complete structured claim and evidence
HLCS rapidly biotinylated the biotin-acceptor fragment of human PC, with transfer limited by enzyme-substrate association.
Human holocarboxylase synthetase / HLCS → Human pyruvate carboxylase / PC source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/22123817.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233", "start_char": 0, "end_char": 1502, "text_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233"}
experimental_model
Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases
exposure
Stopped-flow and quench-flow transfer kinetics
limitations
Fragment kinetics support differential recognition, not a universal nutrient-deficiency survival order in humans.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
This mitochondrial enzyme has a biotin attachment domain recognized by HLCS.
primary_references
[b7-p22123817] Selectivity in post-translational biotin addition to five human carboxylases. (2012). https://pubmed.ncbi.nlm.nih.gov/22123817/ DOI: 10.1074/jbc.m111.275982
tissue_or_cell_type
Purified HLCS and acceptor fragments
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 390–401
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases · source_derived_draft · unverified_draft
### b7-hlcs-pc-acceptor HLCS rapidly biotinylated the biotin-acceptor fragment of human PC, with transfer limited by enzyme-substrate association. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This mitochondrial enzyme has a biotin attachment domain recognized by HLCS. organism: Homo sapiens tissue_or_cell_type: Purified HLCS and acceptor fragments experimental_model: Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases limitations: Fragment kinetics support differential recognition, not a universal nutrient-deficiency survival order in humans. exposure: Stopped-flow and quench-flow transfer kinetics evidence_span: {"source_cache": "artifacts/biotin-research/22123817.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233", "start_char": 0, "end_char": 1502, "text_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233"} [b7-p22123817] Selectivity in post-translational biotin addition to five human carboxylases. (2012). https://pubmed.ncbi.nlm.nih.gov/22123817/ DOI: 10.1074/jbc.m111.275982
Complete structured claim and evidence
HLCS rapidly biotinylated the biotin-acceptor fragment of human PCCA, with transfer limited by enzyme-substrate association.
Human holocarboxylase synthetase / HLCS → Human propionyl-CoA carboxylase alpha subunit / PCCA source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/22123817.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233", "start_char": 0, "end_char": 1502, "text_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233"}
experimental_model
Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases
exposure
Stopped-flow and quench-flow transfer kinetics
limitations
Fragment kinetics support differential recognition, not a universal nutrient-deficiency survival order in humans.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
This mitochondrial enzyme has a biotin attachment domain recognized by HLCS.
primary_references
[b7-p22123817] Selectivity in post-translational biotin addition to five human carboxylases. (2012). https://pubmed.ncbi.nlm.nih.gov/22123817/ DOI: 10.1074/jbc.m111.275982
tissue_or_cell_type
Purified HLCS and acceptor fragments
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 403–414
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases · source_derived_draft · unverified_draft
### b7-hlcs-pcc-acceptor HLCS rapidly biotinylated the biotin-acceptor fragment of human PCCA, with transfer limited by enzyme-substrate association. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This mitochondrial enzyme has a biotin attachment domain recognized by HLCS. organism: Homo sapiens tissue_or_cell_type: Purified HLCS and acceptor fragments experimental_model: Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases limitations: Fragment kinetics support differential recognition, not a universal nutrient-deficiency survival order in humans. exposure: Stopped-flow and quench-flow transfer kinetics evidence_span: {"source_cache": "artifacts/biotin-research/22123817.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233", "start_char": 0, "end_char": 1502, "text_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233"} [b7-p22123817] Selectivity in post-translational biotin addition to five human carboxylases. (2012). https://pubmed.ncbi.nlm.nih.gov/22123817/ DOI: 10.1074/jbc.m111.275982
Complete structured claim and evidence
HLCS rapidly biotinylated the biotin-acceptor fragment of human MCCC1, with transfer limited by enzyme-substrate association.
Human holocarboxylase synthetase / HLCS → Human methylcrotonyl-CoA carboxylase alpha subunit / MCCC1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/22123817.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233", "start_char": 0, "end_char": 1502, "text_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233"}
experimental_model
Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases
exposure
Stopped-flow and quench-flow transfer kinetics
limitations
Fragment kinetics support differential recognition, not a universal nutrient-deficiency survival order in humans.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
This mitochondrial enzyme has a biotin attachment domain recognized by HLCS.
primary_references
[b7-p22123817] Selectivity in post-translational biotin addition to five human carboxylases. (2012). https://pubmed.ncbi.nlm.nih.gov/22123817/ DOI: 10.1074/jbc.m111.275982
tissue_or_cell_type
Purified HLCS and acceptor fragments
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 416–427
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases · source_derived_draft · unverified_draft
### b7-hlcs-mcc-acceptor HLCS rapidly biotinylated the biotin-acceptor fragment of human MCCC1, with transfer limited by enzyme-substrate association. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This mitochondrial enzyme has a biotin attachment domain recognized by HLCS. organism: Homo sapiens tissue_or_cell_type: Purified HLCS and acceptor fragments experimental_model: Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases limitations: Fragment kinetics support differential recognition, not a universal nutrient-deficiency survival order in humans. exposure: Stopped-flow and quench-flow transfer kinetics evidence_span: {"source_cache": "artifacts/biotin-research/22123817.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233", "start_char": 0, "end_char": 1502, "text_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233"} [b7-p22123817] Selectivity in post-translational biotin addition to five human carboxylases. (2012). https://pubmed.ncbi.nlm.nih.gov/22123817/ DOI: 10.1074/jbc.m111.275982
Complete structured claim and evidence
HLCS biotinylation of the human ACACA acceptor fragment was relatively slow and depended hyperbolically on fragment concentration.
Human holocarboxylase synthetase / HLCS → Human acetyl-CoA carboxylase 1 / ACACA source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/22123817.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233", "start_char": 0, "end_char": 1502, "text_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233"}
experimental_model
Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases
exposure
Stopped-flow and quench-flow transfer kinetics
limitations
Fragment kinetics support differential recognition, not a universal nutrient-deficiency survival order in humans.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
The two acetyl-CoA carboxylases showed different attachment kinetics from the mitochondrial carboxylase fragments.
primary_references
[b7-p22123817] Selectivity in post-translational biotin addition to five human carboxylases. (2012). https://pubmed.ncbi.nlm.nih.gov/22123817/ DOI: 10.1074/jbc.m111.275982
tissue_or_cell_type
Purified HLCS and acceptor fragments
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 429–440
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases · source_derived_draft · unverified_draft
### b7-hlcs-acaca-acceptor HLCS biotinylation of the human ACACA acceptor fragment was relatively slow and depended hyperbolically on fragment concentration. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two acetyl-CoA carboxylases showed different attachment kinetics from the mitochondrial carboxylase fragments. organism: Homo sapiens tissue_or_cell_type: Purified HLCS and acceptor fragments experimental_model: Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases limitations: Fragment kinetics support differential recognition, not a universal nutrient-deficiency survival order in humans. exposure: Stopped-flow and quench-flow transfer kinetics evidence_span: {"source_cache": "artifacts/biotin-research/22123817.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233", "start_char": 0, "end_char": 1502, "text_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233"} [b7-p22123817] Selectivity in post-translational biotin addition to five human carboxylases. (2012). https://pubmed.ncbi.nlm.nih.gov/22123817/ DOI: 10.1074/jbc.m111.275982
Complete structured claim and evidence
HLCS biotinylation of the human ACACB acceptor fragment was relatively slow and depended hyperbolically on fragment concentration.
Human holocarboxylase synthetase / HLCS → Human acetyl-CoA carboxylase 2 / ACACB source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/22123817.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233", "start_char": 0, "end_char": 1502, "text_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233"}
experimental_model
Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases
exposure
Stopped-flow and quench-flow transfer kinetics
limitations
Fragment kinetics support differential recognition, not a universal nutrient-deficiency survival order in humans.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
The two acetyl-CoA carboxylases showed different attachment kinetics from the mitochondrial carboxylase fragments.
primary_references
[b7-p22123817] Selectivity in post-translational biotin addition to five human carboxylases. (2012). https://pubmed.ncbi.nlm.nih.gov/22123817/ DOI: 10.1074/jbc.m111.275982
tissue_or_cell_type
Purified HLCS and acceptor fragments
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 442–453
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases · source_derived_draft · unverified_draft
### b7-hlcs-acacb-acceptor HLCS biotinylation of the human ACACB acceptor fragment was relatively slow and depended hyperbolically on fragment concentration. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two acetyl-CoA carboxylases showed different attachment kinetics from the mitochondrial carboxylase fragments. organism: Homo sapiens tissue_or_cell_type: Purified HLCS and acceptor fragments experimental_model: Single-turnover biotin transfer to minimal BCCP fragments from all five human carboxylases limitations: Fragment kinetics support differential recognition, not a universal nutrient-deficiency survival order in humans. exposure: Stopped-flow and quench-flow transfer kinetics evidence_span: {"source_cache": "artifacts/biotin-research/22123817.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233", "start_char": 0, "end_char": 1502, "text_sha256": "559afe20b6f8601a2d055d42fb121c89eaf1ece76afaa5cc0817c20787893233"} [b7-p22123817] Selectivity in post-translational biotin addition to five human carboxylases. (2012). https://pubmed.ncbi.nlm.nih.gov/22123817/ DOI: 10.1074/jbc.m111.275982
Complete structured claim and evidence
The five affected children had serum biotinidase activity at 0–3% of the control mean, with combined carboxylase abnormalities.
Human biotinidase / BTD → Human serum biotinidase activity source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/6883721.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f881dd651d45537377661fc515239c3babb7160c3dbd53b8b0611ba33625aaa", "start_char": 0, "end_char": 1500, "text_sha256": "0f881dd651d45537377661fc515239c3babb7160c3dbd53b8b0611ba33625aaa"}
experimental_model
Serum enzyme assays in 5 children with late-onset multiple carboxylase deficiency and family members
exposure
Inherited deficiency; patient/control comparison
limitations
Early small case series; the serum enzyme phenotype is genetic machinery impairment, not proof of low dietary intake.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
A recycling defect can affect several enzyme pathways at once.
primary_references
[b7-p6883721] Biotinidase deficiency: the enzymatic defect in late-onset multiple carboxylase deficiency. (1983). https://pubmed.ncbi.nlm.nih.gov/6883721/ DOI: 10.1016/0009-8981(83)90096-7
tissue_or_cell_type
Serum and biochemical disease phenotype
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 468–479
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Serum enzyme assays in 5 children with late-onset multiple carboxylase deficiency and family members · source_derived_draft · unverified_draft
### b7-btd-low-activity The five affected children had serum biotinidase activity at 0–3% of the control mean, with combined carboxylase abnormalities. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A recycling defect can affect several enzyme pathways at once. organism: Homo sapiens tissue_or_cell_type: Serum and biochemical disease phenotype experimental_model: Serum enzyme assays in 5 children with late-onset multiple carboxylase deficiency and family members limitations: Early small case series; the serum enzyme phenotype is genetic machinery impairment, not proof of low dietary intake. exposure: Inherited deficiency; patient/control comparison evidence_span: {"source_cache": "artifacts/biotin-research/6883721.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f881dd651d45537377661fc515239c3babb7160c3dbd53b8b0611ba33625aaa", "start_char": 0, "end_char": 1500, "text_sha256": "0f881dd651d45537377661fc515239c3babb7160c3dbd53b8b0611ba33625aaa"} [b7-p6883721] Biotinidase deficiency: the enzymatic defect in late-onset multiple carboxylase deficiency. (1983). https://pubmed.ncbi.nlm.nih.gov/6883721/ DOI: 10.1016/0009-8981(83)90096-7
Complete structured claim and evidence
Biotinidase impairment reduced carboxylase biotinylation and disrupted HLCS and carboxylase expression in the studied human cell model.
Human biotinidase / BTD → Human HLCS expression source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/18845537.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "86a05dc5e8386be649b3f876891503e507217c8f2dd11d9637c67e76effda407", "start_char": 0, "end_char": 1458, "text_sha256": "86a05dc5e8386be649b3f876891503e507217c8f2dd11d9637c67e76effda407"}
experimental_model
Biotinidase-deficient human cell model compared with control cells
exposure
Biotin recycling impairment and biotin repletion experiments
limitations
The proposed brain-protective tissue-allocation mechanism remains an author model, not an established human ranking.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Loss of recycling can affect both cofactor attachment and expression of the attachment machinery.
primary_references
[b7-p18845537] Impaired biotinidase activity disrupts holocarboxylase synthetase expression in late onset multiple carboxylase deficiency. (2008). https://pubmed.ncbi.nlm.nih.gov/18845537/ DOI: 10.1074/jbc.m806985200
tissue_or_cell_type
Cultured patient-derived cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 481–492
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biotinidase-deficient human cell model compared with control cells · source_derived_draft · unverified_draft
### b7-btd-expression Biotinidase impairment reduced carboxylase biotinylation and disrupted HLCS and carboxylase expression in the studied human cell model. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of recycling can affect both cofactor attachment and expression of the attachment machinery. organism: Homo sapiens tissue_or_cell_type: Cultured patient-derived cells experimental_model: Biotinidase-deficient human cell model compared with control cells limitations: The proposed brain-protective tissue-allocation mechanism remains an author model, not an established human ranking. exposure: Biotin recycling impairment and biotin repletion experiments evidence_span: {"source_cache": "artifacts/biotin-research/18845537.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "86a05dc5e8386be649b3f876891503e507217c8f2dd11d9637c67e76effda407", "start_char": 0, "end_char": 1458, "text_sha256": "86a05dc5e8386be649b3f876891503e507217c8f2dd11d9637c67e76effda407"} [b7-p18845537] Impaired biotinidase activity disrupts holocarboxylase synthetase expression in late onset multiple carboxylase deficiency. (2008). https://pubmed.ncbi.nlm.nih.gov/18845537/ DOI: 10.1074/jbc.m806985200
Complete structured claim and evidence
The human HLCS Gly581Ser variant had a biotin Km approximately 45 times the wild-type value.
Human HLCS Gly581Ser variant → Biotin source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/10590022.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bbdc1b8fa77a6935ced529e847093935cf4c8c9e056470e81aa3473968b980c5", "start_char": 0, "end_char": 1628, "text_sha256": "bbdc1b8fa77a6935ced529e847093935cf4c8c9e056470e81aa3473968b980c5"}
experimental_model
Kinetics of seven human HLCS variants, patient cells and clinical response comparison
exposure
Genetic variants and biotin supplementation
limitations
Biotin responsiveness varied with residual enzyme capacity. Genotype effects must not be equated with ordinary dietary biotin deficiency.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
This variant required much more biotin to reach the same fraction of its own maximum rate.
primary_references
[b7-p10590022] Relationship between kinetic properties of mutant enzyme and biochemical and clinical responsiveness to biotin in holocarboxylase synthetase deficiency. (1999). https://pubmed.ncbi.nlm.nih.gov/10590022/ DOI: 10.1203/00006450-199912000-00004
tissue_or_cell_type
Purified variants and cultured patient cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 494–505
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Kinetics of seven human HLCS variants, patient cells and clinical response comparison · source_derived_draft · unverified_draft
### b7-hlcs-g581s The human HLCS Gly581Ser variant had a biotin Km approximately 45 times the wild-type value. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This variant required much more biotin to reach the same fraction of its own maximum rate. organism: Homo sapiens tissue_or_cell_type: Purified variants and cultured patient cells experimental_model: Kinetics of seven human HLCS variants, patient cells and clinical response comparison limitations: Biotin responsiveness varied with residual enzyme capacity. Genotype effects must not be equated with ordinary dietary biotin deficiency. exposure: Genetic variants and biotin supplementation evidence_span: {"source_cache": "artifacts/biotin-research/10590022.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bbdc1b8fa77a6935ced529e847093935cf4c8c9e056470e81aa3473968b980c5", "start_char": 0, "end_char": 1628, "text_sha256": "bbdc1b8fa77a6935ced529e847093935cf4c8c9e056470e81aa3473968b980c5"} [b7-p10590022] Relationship between kinetic properties of mutant enzyme and biochemical and clinical responsiveness to biotin in holocarboxylase synthetase deficiency. (1999). https://pubmed.ncbi.nlm.nih.gov/10590022/ DOI: 10.1203/00006450-199912000-00004
Complete structured claim and evidence
The human HLCS Thr610-deletion variant had a biotin Km approximately three times the wild-type value.
Human HLCS Thr610 deletion variant → Biotin source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/10590022.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bbdc1b8fa77a6935ced529e847093935cf4c8c9e056470e81aa3473968b980c5", "start_char": 0, "end_char": 1628, "text_sha256": "bbdc1b8fa77a6935ced529e847093935cf4c8c9e056470e81aa3473968b980c5"}
experimental_model
Kinetics of seven human HLCS variants, patient cells and clinical response comparison
exposure
Genetic variants and biotin supplementation
limitations
Biotin responsiveness varied with residual enzyme capacity. Genotype effects must not be equated with ordinary dietary biotin deficiency.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Different HLCS variants impair biotin use by different amounts.
primary_references
[b7-p10590022] Relationship between kinetic properties of mutant enzyme and biochemical and clinical responsiveness to biotin in holocarboxylase synthetase deficiency. (1999). https://pubmed.ncbi.nlm.nih.gov/10590022/ DOI: 10.1203/00006450-199912000-00004
tissue_or_cell_type
Purified variants and cultured patient cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 507–518
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Kinetics of seven human HLCS variants, patient cells and clinical response comparison · source_derived_draft · unverified_draft
### b7-hlcs-t610 The human HLCS Thr610-deletion variant had a biotin Km approximately three times the wild-type value. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different HLCS variants impair biotin use by different amounts. organism: Homo sapiens tissue_or_cell_type: Purified variants and cultured patient cells experimental_model: Kinetics of seven human HLCS variants, patient cells and clinical response comparison limitations: Biotin responsiveness varied with residual enzyme capacity. Genotype effects must not be equated with ordinary dietary biotin deficiency. exposure: Genetic variants and biotin supplementation evidence_span: {"source_cache": "artifacts/biotin-research/10590022.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bbdc1b8fa77a6935ced529e847093935cf4c8c9e056470e81aa3473968b980c5", "start_char": 0, "end_char": 1628, "text_sha256": "bbdc1b8fa77a6935ced529e847093935cf4c8c9e056470e81aa3473968b980c5"} [b7-p10590022] Relationship between kinetic properties of mutant enzyme and biochemical and clinical responsiveness to biotin in holocarboxylase synthetase deficiency. (1999). https://pubmed.ncbi.nlm.nih.gov/10590022/ DOI: 10.1203/00006450-199912000-00004
Complete structured claim and evidence
Lower residual HLCS Vmax correlated with poorer PCC and clinical responses to biotin in the studied variants and patients; non-Km variants could also respond.
Human holocarboxylase synthetase / HLCS → Biochemical response to biotin in HLCS deficiency source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/10590022.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bbdc1b8fa77a6935ced529e847093935cf4c8c9e056470e81aa3473968b980c5", "start_char": 0, "end_char": 1628, "text_sha256": "bbdc1b8fa77a6935ced529e847093935cf4c8c9e056470e81aa3473968b980c5"}
experimental_model
Kinetics of seven human HLCS variants, patient cells and clinical response comparison
exposure
Genetic variants and biotin supplementation
limitations
Biotin responsiveness varied with residual enzyme capacity. Genotype effects must not be equated with ordinary dietary biotin deficiency.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
An enzyme with very little remaining capacity may respond less, even when more biotin is supplied.
primary_references
[b7-p10590022] Relationship between kinetic properties of mutant enzyme and biochemical and clinical responsiveness to biotin in holocarboxylase synthetase deficiency. (1999). https://pubmed.ncbi.nlm.nih.gov/10590022/ DOI: 10.1203/00006450-199912000-00004
tissue_or_cell_type
Purified variants and cultured patient cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 520–531
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Kinetics of seven human HLCS variants, patient cells and clinical response comparison · source_derived_draft · unverified_draft
### b7-hlcs-vmax-response Lower residual HLCS Vmax correlated with poorer PCC and clinical responses to biotin in the studied variants and patients; non-Km variants could also respond. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An enzyme with very little remaining capacity may respond less, even when more biotin is supplied. organism: Homo sapiens tissue_or_cell_type: Purified variants and cultured patient cells experimental_model: Kinetics of seven human HLCS variants, patient cells and clinical response comparison limitations: Biotin responsiveness varied with residual enzyme capacity. Genotype effects must not be equated with ordinary dietary biotin deficiency. exposure: Genetic variants and biotin supplementation evidence_span: {"source_cache": "artifacts/biotin-research/10590022.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bbdc1b8fa77a6935ced529e847093935cf4c8c9e056470e81aa3473968b980c5", "start_char": 0, "end_char": 1628, "text_sha256": "bbdc1b8fa77a6935ced529e847093935cf4c8c9e056470e81aa3473968b980c5"} [b7-p10590022] Relationship between kinetic properties of mutant enzyme and biochemical and clinical responsiveness to biotin in holocarboxylase synthetase deficiency. (1999). https://pubmed.ncbi.nlm.nih.gov/10590022/ DOI: 10.1203/00006450-199912000-00004
Complete structured claim and evidence
Newborn-screened children with biotinidase deficiency treated from early life and with good adherence generally had normal physical and cognitive development.
Biotin → Clinical outcome of human biotinidase deficiency source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/25144890.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "462a23bfc98686c02d0d6d92d923de7e05f646daa2e90a3373bde6a251e75f94", "start_char": 0, "end_char": 1414, "text_sha256": "462a23bfc98686c02d0d6d92d923de7e05f646daa2e90a3373bde6a251e75f94"}
experimental_model
Follow-up of 142 newborn-screened children, 22 profound and 120 partial biotinidase deficiency
exposure
Biotin treatment initiated soon after birth
limitations
Observational treated cohort, not a randomized trial or evidence for supplementation of biotin-replete people.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Early identification and treatment of a recycling defect can prevent much of its harm.
primary_references
[b7-p25144890] Outcomes of individuals with profound and partial biotinidase deficiency ascertained by newborn screening in Michigan over 25 years. (2015). https://pubmed.ncbi.nlm.nih.gov/25144890/ DOI: 10.1038/gim.2014.104
tissue_or_cell_type
Clinical development
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 533–544
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Follow-up of 142 newborn-screened children, 22 profound and 120 partial biotinidase deficiency · source_derived_draft · unverified_draft
### b7-btd-early-treatment Newborn-screened children with biotinidase deficiency treated from early life and with good adherence generally had normal physical and cognitive development. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Early identification and treatment of a recycling defect can prevent much of its harm. organism: Homo sapiens tissue_or_cell_type: Clinical development experimental_model: Follow-up of 142 newborn-screened children, 22 profound and 120 partial biotinidase deficiency limitations: Observational treated cohort, not a randomized trial or evidence for supplementation of biotin-replete people. exposure: Biotin treatment initiated soon after birth evidence_span: {"source_cache": "artifacts/biotin-research/25144890.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "462a23bfc98686c02d0d6d92d923de7e05f646daa2e90a3373bde6a251e75f94", "start_char": 0, "end_char": 1414, "text_sha256": "462a23bfc98686c02d0d6d92d923de7e05f646daa2e90a3373bde6a251e75f94"} [b7-p25144890] Outcomes of individuals with profound and partial biotinidase deficiency ascertained by newborn screening in Michigan over 25 years. (2015). https://pubmed.ncbi.nlm.nih.gov/25144890/ DOI: 10.1038/gim.2014.104
Complete structured claim and evidence
Acetyl-CoA-dependent stabilization of human PC triggered ATP hydrolysis and communication between its two reaction centers.
Acetyl-CoA → Human pyruvate carboxylase / PC source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/36283412.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2a5fb8ec1c27e243b8c8ba158f2c58ab1592d9895eecf16438175b2a5778de15", "start_char": 0, "end_char": 1060, "text_sha256": "2a5fb8ec1c27e243b8c8ba158f2c58ab1592d9895eecf16438175b2a5778de15"}
experimental_model
Time-resolved cryo-EM and biochemical analysis of human PC
exposure
Pyruvate, ATP and acetyl-CoA catalytic conditions
limitations
Purified-enzyme regulation is not evidence that consuming B5 or biotin stimulates this pathway in every tissue.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
The biotin-carrying enzyme coordinates two reaction stations rather than performing one isolated chemical step.
primary_references
[b7-p36283412] Mechanistic insight into allosteric activation of human pyruvate carboxylase by acetyl-CoA. (2022). https://pubmed.ncbi.nlm.nih.gov/36283412/ DOI: 10.1016/j.molcel.2022.09.033
tissue_or_cell_type
Purified human pyruvate carboxylase
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 572–583
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-resolved cryo-EM and biochemical analysis of human PC · source_derived_draft · unverified_draft
### b7-pc-communication Acetyl-CoA-dependent stabilization of human PC triggered ATP hydrolysis and communication between its two reaction centers. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The biotin-carrying enzyme coordinates two reaction stations rather than performing one isolated chemical step. organism: Homo sapiens tissue_or_cell_type: Purified human pyruvate carboxylase experimental_model: Time-resolved cryo-EM and biochemical analysis of human PC limitations: Purified-enzyme regulation is not evidence that consuming B5 or biotin stimulates this pathway in every tissue. exposure: Pyruvate, ATP and acetyl-CoA catalytic conditions evidence_span: {"source_cache": "artifacts/biotin-research/36283412.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2a5fb8ec1c27e243b8c8ba158f2c58ab1592d9895eecf16438175b2a5778de15", "start_char": 0, "end_char": 1060, "text_sha256": "2a5fb8ec1c27e243b8c8ba158f2c58ab1592d9895eecf16438175b2a5778de15"} [b7-p36283412] Mechanistic insight into allosteric activation of human pyruvate carboxylase by acetyl-CoA. (2022). https://pubmed.ncbi.nlm.nih.gov/36283412/ DOI: 10.1016/j.molcel.2022.09.033
Complete structured claim and evidence
The human PC C-terminal structure displayed a conserved tetrameric arrangement, with a PC tetramerization domain identified by structural and mutagenesis analysis.
Human pyruvate carboxylase / PC → Human pyruvate carboxylase / PC source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/18297087.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "64ad42b855e8e31bb8103ad2740baab36988d47779218fbbf19b13f34f4a4d10", "start_char": 0, "end_char": 1026, "text_sha256": "64ad42b855e8e31bb8103ad2740baab36988d47779218fbbf19b13f34f4a4d10"}
experimental_model
Crystal structures of human PC lacking the BC domain and full-length S. aureus PC; mutagenesis
exposure
Structural and mutagenesis experiments
limitations
The human structure was a C-terminal fragment, not intact human PC; bacterial domain positions must not be silently assigned to human enzyme.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens; Staphylococcus aureus
plain_language
Enzyme assembly matters as well as the availability of biotin.
primary_references
[b7-p18297087] Crystal structures of human and Staphylococcus aureus pyruvate carboxylase and molecular insights into the carboxyltransfer reaction. (2008). https://pubmed.ncbi.nlm.nih.gov/18297087/ DOI: 10.1038/nsmb.1393
tissue_or_cell_type
Purified proteins
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 585–596
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Crystal structures of human PC lacking the BC domain and full-length S. aureus PC; mutagenesis · source_derived_draft · unverified_draft
### b7-pc-tetramer The human PC C-terminal structure displayed a conserved tetrameric arrangement, with a PC tetramerization domain identified by structural and mutagenesis analysis. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Enzyme assembly matters as well as the availability of biotin. organism: Homo sapiens; Staphylococcus aureus tissue_or_cell_type: Purified proteins experimental_model: Crystal structures of human PC lacking the BC domain and full-length S. aureus PC; mutagenesis limitations: The human structure was a C-terminal fragment, not intact human PC; bacterial domain positions must not be silently assigned to human enzyme. exposure: Structural and mutagenesis experiments evidence_span: {"source_cache": "artifacts/biotin-research/18297087.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "64ad42b855e8e31bb8103ad2740baab36988d47779218fbbf19b13f34f4a4d10", "start_char": 0, "end_char": 1026, "text_sha256": "64ad42b855e8e31bb8103ad2740baab36988d47779218fbbf19b13f34f4a4d10"} [b7-p18297087] Crystal structures of human and Staphylococcus aureus pyruvate carboxylase and molecular insights into the carboxyltransfer reaction. (2008). https://pubmed.ncbi.nlm.nih.gov/18297087/ DOI: 10.1038/nsmb.1393
Complete structured claim and evidence
PCCA contains the biotin-carboxylase and biotin-carrier domains of human PCC.
Human propionyl-CoA carboxylase alpha subunit / PCCA → Human propionyl-CoA carboxylase / PCC source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/20725044.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "825bf28b9f35a8d45f8d08d883fa200bd430336b0558db035ce4fd1c5ef19053", "start_char": 0, "end_char": 1921, "text_sha256": "825bf28b9f35a8d45f8d08d883fa200bd430336b0558db035ce4fd1c5ef19053"}
experimental_model
Bacterial PCC crystallography and separate 15-angstrom human PCC cryo-EM reconstruction
exposure
Structural analysis
limitations
Atomic bacterial positions are not high-resolution human measurements. Human cryo-EM establishes the overall assembly at lower resolution.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens; bacterial PCC comparison
plain_language
The alpha subunit handles biotin loading with the carboxyl group and carries that group onward.
primary_references
[b7-p20725044] Crystal structure of the alpha(6)beta(6) holoenzyme of propionyl-coenzyme A carboxylase. (2010). https://pubmed.ncbi.nlm.nih.gov/20725044/ DOI: 10.1038/nature09302
tissue_or_cell_type
Purified PCC complexes
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 598–609
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Bacterial PCC crystallography and separate 15-angstrom human PCC cryo-EM reconstruction · source_derived_draft · unverified_draft
### b7-pcc-pcca PCCA contains the biotin-carboxylase and biotin-carrier domains of human PCC. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The alpha subunit handles biotin loading with the carboxyl group and carries that group onward. organism: Homo sapiens; bacterial PCC comparison tissue_or_cell_type: Purified PCC complexes experimental_model: Bacterial PCC crystallography and separate 15-angstrom human PCC cryo-EM reconstruction limitations: Atomic bacterial positions are not high-resolution human measurements. Human cryo-EM establishes the overall assembly at lower resolution. exposure: Structural analysis evidence_span: {"source_cache": "artifacts/biotin-research/20725044.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "825bf28b9f35a8d45f8d08d883fa200bd430336b0558db035ce4fd1c5ef19053", "start_char": 0, "end_char": 1921, "text_sha256": "825bf28b9f35a8d45f8d08d883fa200bd430336b0558db035ce4fd1c5ef19053"} [b7-p20725044] Crystal structure of the alpha(6)beta(6) holoenzyme of propionyl-coenzyme A carboxylase. (2010). https://pubmed.ncbi.nlm.nih.gov/20725044/ DOI: 10.1038/nature09302
Complete structured claim and evidence
PCCB provides the carboxyltransferase activity of human PCC.
Human propionyl-CoA carboxylase beta subunit / PCCB → Human propionyl-CoA carboxylase / PCC source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/20725044.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "825bf28b9f35a8d45f8d08d883fa200bd430336b0558db035ce4fd1c5ef19053", "start_char": 0, "end_char": 1921, "text_sha256": "825bf28b9f35a8d45f8d08d883fa200bd430336b0558db035ce4fd1c5ef19053"}
experimental_model
Bacterial PCC crystallography and separate 15-angstrom human PCC cryo-EM reconstruction
exposure
Structural analysis
limitations
Atomic bacterial positions are not high-resolution human measurements. Human cryo-EM establishes the overall assembly at lower resolution.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens; bacterial PCC comparison
plain_language
The beta subunit performs the transfer onto the carbon substrate.
primary_references
[b7-p20725044] Crystal structure of the alpha(6)beta(6) holoenzyme of propionyl-coenzyme A carboxylase. (2010). https://pubmed.ncbi.nlm.nih.gov/20725044/ DOI: 10.1038/nature09302
tissue_or_cell_type
Purified PCC complexes
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 611–622
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Bacterial PCC crystallography and separate 15-angstrom human PCC cryo-EM reconstruction · source_derived_draft · unverified_draft
### b7-pcc-pccb PCCB provides the carboxyltransferase activity of human PCC. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The beta subunit performs the transfer onto the carbon substrate. organism: Homo sapiens; bacterial PCC comparison tissue_or_cell_type: Purified PCC complexes experimental_model: Bacterial PCC crystallography and separate 15-angstrom human PCC cryo-EM reconstruction limitations: Atomic bacterial positions are not high-resolution human measurements. Human cryo-EM establishes the overall assembly at lower resolution. exposure: Structural analysis evidence_span: {"source_cache": "artifacts/biotin-research/20725044.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "825bf28b9f35a8d45f8d08d883fa200bd430336b0558db035ce4fd1c5ef19053", "start_char": 0, "end_char": 1921, "text_sha256": "825bf28b9f35a8d45f8d08d883fa200bd430336b0558db035ce4fd1c5ef19053"} [b7-p20725044] Crystal structure of the alpha(6)beta(6) holoenzyme of propionyl-coenzyme A carboxylase. (2010). https://pubmed.ncbi.nlm.nih.gov/20725044/ DOI: 10.1038/nature09302
Complete structured claim and evidence
Human PCC cryo-EM supported an alpha6-beta6 assembly similar to the bacterial holoenzyme architecture.
Human propionyl-CoA carboxylase / PCC → Human propionyl-CoA carboxylase alpha subunit / PCCA source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/20725044.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "825bf28b9f35a8d45f8d08d883fa200bd430336b0558db035ce4fd1c5ef19053", "start_char": 0, "end_char": 1921, "text_sha256": "825bf28b9f35a8d45f8d08d883fa200bd430336b0558db035ce4fd1c5ef19053"}
experimental_model
Bacterial PCC crystallography and separate 15-angstrom human PCC cryo-EM reconstruction
exposure
Structural analysis
limitations
Atomic bacterial positions are not high-resolution human measurements. Human cryo-EM establishes the overall assembly at lower resolution.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens; bacterial PCC comparison
plain_language
Six alpha and six beta subunits form the working complex.
primary_references
[b7-p20725044] Crystal structure of the alpha(6)beta(6) holoenzyme of propionyl-coenzyme A carboxylase. (2010). https://pubmed.ncbi.nlm.nih.gov/20725044/ DOI: 10.1038/nature09302
tissue_or_cell_type
Purified PCC complexes
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 624–635
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Bacterial PCC crystallography and separate 15-angstrom human PCC cryo-EM reconstruction · source_derived_draft · unverified_draft
### b7-pcc-assembly Human PCC cryo-EM supported an alpha6-beta6 assembly similar to the bacterial holoenzyme architecture. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Six alpha and six beta subunits form the working complex. organism: Homo sapiens; bacterial PCC comparison tissue_or_cell_type: Purified PCC complexes experimental_model: Bacterial PCC crystallography and separate 15-angstrom human PCC cryo-EM reconstruction limitations: Atomic bacterial positions are not high-resolution human measurements. Human cryo-EM establishes the overall assembly at lower resolution. exposure: Structural analysis evidence_span: {"source_cache": "artifacts/biotin-research/20725044.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "825bf28b9f35a8d45f8d08d883fa200bd430336b0558db035ce4fd1c5ef19053", "start_char": 0, "end_char": 1921, "text_sha256": "825bf28b9f35a8d45f8d08d883fa200bd430336b0558db035ce4fd1c5ef19053"} [b7-p20725044] Crystal structure of the alpha(6)beta(6) holoenzyme of propionyl-coenzyme A carboxylase. (2010). https://pubmed.ncbi.nlm.nih.gov/20725044/ DOI: 10.1038/nature09302
Complete structured claim and evidence
The human ACC1 biotin-carrier domain contains biotin covalently attached to Lys786.
Human acetyl-CoA carboxylase 1 / ACACA → Human ACC1 biotinylated at Lys786 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/39383219.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5f7d3cd6a5865a03b8dc9c510f60249ee2c9f6516773780e5d7b4aef0a9b2db8", "start_char": 17700, "end_char": 18021, "text_sha256": "577b5c24795f7637a47e725c7e87ae9632c6aa96e74424b66d14ccd76a87e3bb"}
experimental_model
Cryo-EM of endogenous and recombinant human ACC1 filaments
exposure
Inactive substrate-containing and dephosphorylated/citrate-treated states
limitations
Filament presence alone does not mean enzyme activation; the paper resolved both active and inactive arrangements.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Biotin is attached at a specific amino-acid site on ACC1.
primary_references
[b7-p39383219] Filament structures unveil the dynamic organization of human acetyl-CoA carboxylase. (2024). https://pubmed.ncbi.nlm.nih.gov/39383219/ DOI: 10.1126/sciadv.ado4880
tissue_or_cell_type
Purified human ACC1
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 650–661
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of endogenous and recombinant human ACC1 filaments · source_derived_draft · unverified_draft
### b7-acc1-k786 The human ACC1 biotin-carrier domain contains biotin covalently attached to Lys786. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Biotin is attached at a specific amino-acid site on ACC1. organism: Homo sapiens tissue_or_cell_type: Purified human ACC1 experimental_model: Cryo-EM of endogenous and recombinant human ACC1 filaments limitations: Filament presence alone does not mean enzyme activation; the paper resolved both active and inactive arrangements. exposure: Inactive substrate-containing and dephosphorylated/citrate-treated states evidence_span: {"source_cache": "artifacts/biotin-research/39383219.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5f7d3cd6a5865a03b8dc9c510f60249ee2c9f6516773780e5d7b4aef0a9b2db8", "start_char": 17700, "end_char": 18021, "text_sha256": "577b5c24795f7637a47e725c7e87ae9632c6aa96e74424b66d14ccd76a87e3bb"} [b7-p39383219] Filament structures unveil the dynamic organization of human acetyl-CoA carboxylase. (2024). https://pubmed.ncbi.nlm.nih.gov/39383219/ DOI: 10.1126/sciadv.ado4880
Complete structured claim and evidence
Dephosphorylation and citrate treatment produced the activated human ACC1 filament state resolved by cryo-EM.
Citrate → Human acetyl-CoA carboxylase 1 / ACACA source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/39383219.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7fa420ace21cebdb778923fbf951a99c035c9fae2af8f4876becf672947d9242", "start_char": 0, "end_char": 863, "text_sha256": "7fa420ace21cebdb778923fbf951a99c035c9fae2af8f4876becf672947d9242"}
experimental_model
Cryo-EM of endogenous and recombinant human ACC1 filaments
exposure
Inactive substrate-containing and dephosphorylated/citrate-treated states
limitations
Filament presence alone does not mean enzyme activation; the paper resolved both active and inactive arrangements.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
ACC1 needs appropriate regulation as well as its vitamin cofactor.
primary_references
[b7-p39383219] Filament structures unveil the dynamic organization of human acetyl-CoA carboxylase. (2024). https://pubmed.ncbi.nlm.nih.gov/39383219/ DOI: 10.1126/sciadv.ado4880
tissue_or_cell_type
Purified human ACC1
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 663–674
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of endogenous and recombinant human ACC1 filaments · source_derived_draft · unverified_draft
### b7-acc1-active-state Dephosphorylation and citrate treatment produced the activated human ACC1 filament state resolved by cryo-EM. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: ACC1 needs appropriate regulation as well as its vitamin cofactor. organism: Homo sapiens tissue_or_cell_type: Purified human ACC1 experimental_model: Cryo-EM of endogenous and recombinant human ACC1 filaments limitations: Filament presence alone does not mean enzyme activation; the paper resolved both active and inactive arrangements. exposure: Inactive substrate-containing and dephosphorylated/citrate-treated states evidence_span: {"source_cache": "artifacts/biotin-research/39383219.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7fa420ace21cebdb778923fbf951a99c035c9fae2af8f4876becf672947d9242", "start_char": 0, "end_char": 863, "text_sha256": "7fa420ace21cebdb778923fbf951a99c035c9fae2af8f4876becf672947d9242"} [b7-p39383219] Filament structures unveil the dynamic organization of human acetyl-CoA carboxylase. (2024). https://pubmed.ncbi.nlm.nih.gov/39383219/ DOI: 10.1126/sciadv.ado4880
Complete structured claim and evidence
Citrate increased recombinant human ACC2 kcat and kcat/Km for ATP and acetyl-CoA.
Citrate → Human acetyl-CoA carboxylase 2 / ACACB source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/19236960.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bedd791235b10ff5942ef7177b54bca5b2243883da02fb24572691aaf5975be5", "start_char": 0, "end_char": 896, "text_sha256": "bedd791235b10ff5942ef7177b54bca5b2243883da02fb24572691aaf5975be5"}
experimental_model
Steady-state kinetics of purified recombinant human ACC2; LC-MS/MS malonyl-CoA assay
exposure
Bicarbonate, ATP, acetyl-CoA and citrate concentration matrices
limitations
Kinetic constants are assay properties; they do not define a dietary biotin or B5 threshold.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Citrate affects both enzyme speed and effective substrate use.
primary_references
[b7-p19236960] Characterization of recombinant human acetyl-CoA carboxylase-2 steady-state kinetics. (2009). https://pubmed.ncbi.nlm.nih.gov/19236960/ DOI: 10.1016/j.bbapap.2009.02.004
tissue_or_cell_type
Purified human ACC2
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 689–700
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Steady-state kinetics of purified recombinant human ACC2; LC-MS/MS malonyl-CoA assay · source_derived_draft · unverified_draft
### b7-acc2-citrate Citrate increased recombinant human ACC2 kcat and kcat/Km for ATP and acetyl-CoA. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Citrate affects both enzyme speed and effective substrate use. organism: Homo sapiens tissue_or_cell_type: Purified human ACC2 experimental_model: Steady-state kinetics of purified recombinant human ACC2; LC-MS/MS malonyl-CoA assay limitations: Kinetic constants are assay properties; they do not define a dietary biotin or B5 threshold. exposure: Bicarbonate, ATP, acetyl-CoA and citrate concentration matrices evidence_span: {"source_cache": "artifacts/biotin-research/19236960.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bedd791235b10ff5942ef7177b54bca5b2243883da02fb24572691aaf5975be5", "start_char": 0, "end_char": 896, "text_sha256": "bedd791235b10ff5942ef7177b54bca5b2243883da02fb24572691aaf5975be5"} [b7-p19236960] Characterization of recombinant human acetyl-CoA carboxylase-2 steady-state kinetics. (2009). https://pubmed.ncbi.nlm.nih.gov/19236960/ DOI: 10.1016/j.bbapap.2009.02.004
Complete structured claim and evidence
In the studied human ACC2 domain, phosphorylated Ser222 occupied the putative dimer interface, disrupting polymerization and explaining AMPK-mediated inactivation.
AMP-activated protein kinase complexes → Human acetyl-CoA carboxylase 2 / ACACB source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/19900410.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3d7161fb1a281c68bbe3b8d4738b26d5ed762ca2bea3d9621ee6c8946a7fa71c", "start_char": 0, "end_char": 870, "text_sha256": "3d7161fb1a281c68bbe3b8d4738b26d5ed762ca2bea3d9621ee6c8946a7fa71c"}
experimental_model
Crystal structures of the human ACC2 biotin-carboxylase domain after AMPK phosphorylation
exposure
Phosphorylation and soraphen A comparison
limitations
Domain structures explain a regulatory mechanism; the construct uses Ser222 numbering and must not be silently relabeled with another isoform numbering scheme.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
An energy-sensing kinase can switch ACC2 down even when biotin is available.
primary_references
[b7-p19900410] Molecular mechanism for the regulation of human ACC2 through phosphorylation by AMPK. (2010). https://pubmed.ncbi.nlm.nih.gov/19900410/ DOI: 10.1016/j.bbrc.2009.11.029
tissue_or_cell_type
Purified ACC2 domain
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 702–713
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Crystal structures of the human ACC2 biotin-carboxylase domain after AMPK phosphorylation · source_derived_draft · unverified_draft
### b7-acc2-ampk In the studied human ACC2 domain, phosphorylated Ser222 occupied the putative dimer interface, disrupting polymerization and explaining AMPK-mediated inactivation. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An energy-sensing kinase can switch ACC2 down even when biotin is available. organism: Homo sapiens tissue_or_cell_type: Purified ACC2 domain experimental_model: Crystal structures of the human ACC2 biotin-carboxylase domain after AMPK phosphorylation limitations: Domain structures explain a regulatory mechanism; the construct uses Ser222 numbering and must not be silently relabeled with another isoform numbering scheme. exposure: Phosphorylation and soraphen A comparison evidence_span: {"source_cache": "artifacts/biotin-research/19900410.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3d7161fb1a281c68bbe3b8d4738b26d5ed762ca2bea3d9621ee6c8946a7fa71c", "start_char": 0, "end_char": 870, "text_sha256": "3d7161fb1a281c68bbe3b8d4738b26d5ed762ca2bea3d9621ee6c8946a7fa71c"} [b7-p19900410] Molecular mechanism for the regulation of human ACC2 through phosphorylation by AMPK. (2010). https://pubmed.ncbi.nlm.nih.gov/19900410/ DOI: 10.1016/j.bbrc.2009.11.029
Complete structured claim and evidence
Acacb-null mice had approximately 30-fold lower muscle malonyl-CoA and 10-fold lower heart malonyl-CoA than wild-type mice.
Acacb-null mouse genotype → Mouse muscle malonyl-CoA concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/11283375.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249", "start_char": 0, "end_char": 894, "text_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249"}
experimental_model
Acacb-knockout mice compared with wild type
exposure
Genetic deletion
limitations
Loss of one enzyme in mice is not dietary biotin deficiency, which can affect several enzymes; this is not evidence for inducing deficiency to change body weight.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Mus musculus
plain_language
Loss of ACC2 lowered the local metabolite that helps restrain fatty-acid entry.
primary_references
[b7-p11283375] Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2. (2001). https://pubmed.ncbi.nlm.nih.gov/11283375/ DOI: 10.1126/science.1056843
tissue_or_cell_type
Heart, skeletal muscle and adipose tissue
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 715–726
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acacb-knockout mice compared with wild type · source_derived_draft · unverified_draft
### b7-acc2-null-malonyl Acacb-null mice had approximately 30-fold lower muscle malonyl-CoA and 10-fold lower heart malonyl-CoA than wild-type mice. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of ACC2 lowered the local metabolite that helps restrain fatty-acid entry. organism: Mus musculus tissue_or_cell_type: Heart, skeletal muscle and adipose tissue experimental_model: Acacb-knockout mice compared with wild type limitations: Loss of one enzyme in mice is not dietary biotin deficiency, which can affect several enzymes; this is not evidence for inducing deficiency to change body weight. exposure: Genetic deletion evidence_span: {"source_cache": "artifacts/biotin-research/11283375.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249", "start_char": 0, "end_char": 894, "text_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249"} [b7-p11283375] Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2. (2001). https://pubmed.ncbi.nlm.nih.gov/11283375/ DOI: 10.1126/science.1056843
Complete structured claim and evidence
Soleus fatty-acid oxidation was about 30% higher in Acacb-null mice than in wild-type mice.
Acacb-null mouse genotype → Mouse muscle fatty-acid oxidation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/11283375.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249", "start_char": 0, "end_char": 894, "text_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249"}
experimental_model
Acacb-knockout mice compared with wild type
exposure
Genetic deletion
limitations
Loss of one enzyme in mice is not dietary biotin deficiency, which can affect several enzymes; this is not evidence for inducing deficiency to change body weight.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Mus musculus
plain_language
The enzyme deletion changed fuel use in mouse muscle.
primary_references
[b7-p11283375] Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2. (2001). https://pubmed.ncbi.nlm.nih.gov/11283375/ DOI: 10.1126/science.1056843
tissue_or_cell_type
Heart, skeletal muscle and adipose tissue
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 728–739
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acacb-knockout mice compared with wild type · source_derived_draft · unverified_draft
### b7-acc2-null-oxidation Soleus fatty-acid oxidation was about 30% higher in Acacb-null mice than in wild-type mice. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The enzyme deletion changed fuel use in mouse muscle. organism: Mus musculus tissue_or_cell_type: Heart, skeletal muscle and adipose tissue experimental_model: Acacb-knockout mice compared with wild type limitations: Loss of one enzyme in mice is not dietary biotin deficiency, which can affect several enzymes; this is not evidence for inducing deficiency to change body weight. exposure: Genetic deletion evidence_span: {"source_cache": "artifacts/biotin-research/11283375.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249", "start_char": 0, "end_char": 894, "text_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249"} [b7-p11283375] Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2. (2001). https://pubmed.ncbi.nlm.nih.gov/11283375/ DOI: 10.1126/science.1056843
Complete structured claim and evidence
Deleting the first 28 residues of human CPT1B removed high-affinity malonyl-CoA binding and inhibition despite retained catalytic activity.
Human CPT1B N-terminal 28-residue deletion → Malonyl-CoA source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/10651636.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e99728ef83700f17a810421385b71ea243576419df807dc4749b588beb01d400", "start_char": 0, "end_char": 1542, "text_sha256": "e99728ef83700f17a810421385b71ea243576419df807dc4749b588beb01d400"}
experimental_model
Human CPT1B wild type and N-terminal deletions expressed in yeast mitochondria
exposure
Malonyl-CoA binding and activity assays
limitations
Expression host is yeast; these data concern human CPT1B, not every CPT1 isoform or a biotin supplementation outcome.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
This engineered change separates the enzyme brake from its basic catalytic function.
primary_references
[b7-p10651636] The first 28 N-terminal amino acid residues of human heart muscle carnitine palmitoyltransferase I are essential for malonyl CoA sensitivity and high-affinity binding. (2000). https://pubmed.ncbi.nlm.nih.gov/10651636/ DOI: 10.1021/bi9918700
tissue_or_cell_type
Recombinant human muscle/heart CPT1B
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 754–765
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CPT1B wild type and N-terminal deletions expressed in yeast mitochondria · source_derived_draft · unverified_draft
### b7-cpt1b-delta28 Deleting the first 28 residues of human CPT1B removed high-affinity malonyl-CoA binding and inhibition despite retained catalytic activity. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This engineered change separates the enzyme brake from its basic catalytic function. organism: Homo sapiens tissue_or_cell_type: Recombinant human muscle/heart CPT1B experimental_model: Human CPT1B wild type and N-terminal deletions expressed in yeast mitochondria limitations: Expression host is yeast; these data concern human CPT1B, not every CPT1 isoform or a biotin supplementation outcome. exposure: Malonyl-CoA binding and activity assays evidence_span: {"source_cache": "artifacts/biotin-research/10651636.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e99728ef83700f17a810421385b71ea243576419df807dc4749b588beb01d400", "start_char": 0, "end_char": 1542, "text_sha256": "e99728ef83700f17a810421385b71ea243576419df807dc4749b588beb01d400"} [b7-p10651636] The first 28 N-terminal amino acid residues of human heart muscle carnitine palmitoyltransferase I are essential for malonyl CoA sensitivity and high-affinity binding. (2000). https://pubmed.ncbi.nlm.nih.gov/10651636/ DOI: 10.1021/bi9918700
Complete structured claim and evidence
Active recombinant human MCC contained alpha and beta subunits at a one-to-one ratio.
Human methylcrotonyl-CoA carboxylase alpha subunit / MCCC1 → Human methylcrotonyl-CoA carboxylase beta subunit / MCCC2 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/17360195.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ae046490d9657d005d5c39efb1f7439bc015d0cb2190834e3e868de70eaf985", "start_char": 0, "end_char": 1067, "text_sha256": "3ae046490d9657d005d5c39efb1f7439bc015d0cb2190834e3e868de70eaf985"}
experimental_model
Purified recombinant human MCC produced by baculovirus expression
exposure
ATP and methylcrotonyl-CoA kinetics
limitations
Recombinant-enzyme kinetics do not determine human dietary requirements.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
MCC needs both subunits; biotin cannot replace a missing protein partner.
primary_references
[b7-p17360195] Expression, purification, characterization of human 3-methylcrotonyl-CoA carboxylase (MCCC). (2007). https://pubmed.ncbi.nlm.nih.gov/17360195/ DOI: 10.1016/j.pep.2007.01.012
tissue_or_cell_type
Purified human MCC complex
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 767–778
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human MCC produced by baculovirus expression · source_derived_draft · unverified_draft
### b7-mcc-complex Active recombinant human MCC contained alpha and beta subunits at a one-to-one ratio. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: MCC needs both subunits; biotin cannot replace a missing protein partner. organism: Homo sapiens tissue_or_cell_type: Purified human MCC complex experimental_model: Purified recombinant human MCC produced by baculovirus expression limitations: Recombinant-enzyme kinetics do not determine human dietary requirements. exposure: ATP and methylcrotonyl-CoA kinetics evidence_span: {"source_cache": "artifacts/biotin-research/17360195.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ae046490d9657d005d5c39efb1f7439bc015d0cb2190834e3e868de70eaf985", "start_char": 0, "end_char": 1067, "text_sha256": "3ae046490d9657d005d5c39efb1f7439bc015d0cb2190834e3e868de70eaf985"} [b7-p17360195] Expression, purification, characterization of human 3-methylcrotonyl-CoA carboxylase (MCCC). (2007). https://pubmed.ncbi.nlm.nih.gov/17360195/ DOI: 10.1016/j.pep.2007.01.012
Complete structured claim and evidence
Recombinant human MCC had an ATP Km of 45 ± 11 micromolar and a methylcrotonyl-CoA Km of 74 ± 7 micromolar.
Human 3-methylcrotonyl-CoA carboxylase complex → ATP source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/17360195.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ae046490d9657d005d5c39efb1f7439bc015d0cb2190834e3e868de70eaf985", "start_char": 0, "end_char": 1067, "text_sha256": "3ae046490d9657d005d5c39efb1f7439bc015d0cb2190834e3e868de70eaf985"}
experimental_model
Purified recombinant human MCC produced by baculovirus expression
exposure
ATP and methylcrotonyl-CoA kinetics
limitations
Recombinant-enzyme kinetics do not determine human dietary requirements.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
The biotin-dependent reaction also requires an energy substrate and the carbon substrate.
primary_references
[b7-p17360195] Expression, purification, characterization of human 3-methylcrotonyl-CoA carboxylase (MCCC). (2007). https://pubmed.ncbi.nlm.nih.gov/17360195/ DOI: 10.1016/j.pep.2007.01.012
tissue_or_cell_type
Purified human MCC complex
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 780–791
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human MCC produced by baculovirus expression · source_derived_draft · unverified_draft
### b7-mcc-atp Recombinant human MCC had an ATP Km of 45 ± 11 micromolar and a methylcrotonyl-CoA Km of 74 ± 7 micromolar. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The biotin-dependent reaction also requires an energy substrate and the carbon substrate. organism: Homo sapiens tissue_or_cell_type: Purified human MCC complex experimental_model: Purified recombinant human MCC produced by baculovirus expression limitations: Recombinant-enzyme kinetics do not determine human dietary requirements. exposure: ATP and methylcrotonyl-CoA kinetics evidence_span: {"source_cache": "artifacts/biotin-research/17360195.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ae046490d9657d005d5c39efb1f7439bc015d0cb2190834e3e868de70eaf985", "start_char": 0, "end_char": 1067, "text_sha256": "3ae046490d9657d005d5c39efb1f7439bc015d0cb2190834e3e868de70eaf985"} [b7-p17360195] Expression, purification, characterization of human 3-methylcrotonyl-CoA carboxylase (MCCC). (2007). https://pubmed.ncbi.nlm.nih.gov/17360195/ DOI: 10.1016/j.pep.2007.01.012
Complete structured claim and evidence
Structural comparisons supported substrate-dependent, coordinated activation of human MCC.
3-Methylcrotonyl-CoA → Human 3-methylcrotonyl-CoA carboxylase complex source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/39223421.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "221115ee36b8452b3915e000ae5f363f8f771705dcbb17570343b8f536b7c87a", "start_char": 0, "end_char": 1050, "text_sha256": "221115ee36b8452b3915e000ae5f363f8f771705dcbb17570343b8f536b7c87a"}
experimental_model
Structures of purified endogenous human MCC, PCC and PC; substrate-bound MCC conformations
exposure
Cryo-EM and substrate-bound structural analysis
limitations
Indexed abstract and publisher preview inspected; detailed residue-level claims require full-paper review. Published online 2024, journal issue 2025.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Adding substrate reorganizes the working enzyme; the word synergy here refers to enzyme parts, not proven synergy between supplements.
primary_references
[b7-p39223421] Structural insight into synergistic activation of human 3-methylcrotonyl-CoA carboxylase. (2025). https://pubmed.ncbi.nlm.nih.gov/39223421/ DOI: 10.1038/s41594-024-01379-3
tissue_or_cell_type
Purified endogenous mitochondrial carboxylases
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 806–817
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Structures of purified endogenous human MCC, PCC and PC; substrate-bound MCC conformations · source_derived_draft · unverified_draft
### b7-mcc-substrate-conformations Structural comparisons supported substrate-dependent, coordinated activation of human MCC. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding substrate reorganizes the working enzyme; the word synergy here refers to enzyme parts, not proven synergy between supplements. organism: Homo sapiens tissue_or_cell_type: Purified endogenous mitochondrial carboxylases experimental_model: Structures of purified endogenous human MCC, PCC and PC; substrate-bound MCC conformations limitations: Indexed abstract and publisher preview inspected; detailed residue-level claims require full-paper review. Published online 2024, journal issue 2025. exposure: Cryo-EM and substrate-bound structural analysis evidence_span: {"source_cache": "artifacts/biotin-research/39223421.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "221115ee36b8452b3915e000ae5f363f8f771705dcbb17570343b8f536b7c87a", "start_char": 0, "end_char": 1050, "text_sha256": "221115ee36b8452b3915e000ae5f363f8f771705dcbb17570343b8f536b7c87a"} [b7-p39223421] Structural insight into synergistic activation of human 3-methylcrotonyl-CoA carboxylase. (2025). https://pubmed.ncbi.nlm.nih.gov/39223421/ DOI: 10.1038/s41594-024-01379-3
Complete structured claim and evidence
Liver-specific Pcx deletion reduced hepatic anaplerosis, TCA-cycle intermediates and gluconeogenesis.
Liver-specific Pcx-null mouse genotype → Mouse hepatic gluconeogenesis source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/31006591.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e", "start_char": 0, "end_char": 1141, "text_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e"}
experimental_model
Liver-specific Pcx-knockout mice
exposure
Genetic deletion of hepatic pyruvate carboxylase
limitations
Genetic enzyme deletion is not a dietary biotin experiment. Cross-nutrient implications identify pathway dependence rather than a proven supplement response.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Mus musculus
plain_language
PC helps replenish the carbon pool needed for glucose production.
primary_references
[b7-p31006591] Pyruvate-Carboxylase-Mediated Anaplerosis Promotes Antioxidant Capacity by Sustaining TCA Cycle and Redox Metabolism in Liver. (2019). https://pubmed.ncbi.nlm.nih.gov/31006591/ DOI: 10.1016/j.cmet.2019.03.014
tissue_or_cell_type
Liver and systemic metabolism
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 819–830
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Liver-specific Pcx-knockout mice · source_derived_draft · unverified_draft
### b7-pc-null-gluconeogenesis Liver-specific Pcx deletion reduced hepatic anaplerosis, TCA-cycle intermediates and gluconeogenesis. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: PC helps replenish the carbon pool needed for glucose production. organism: Mus musculus tissue_or_cell_type: Liver and systemic metabolism experimental_model: Liver-specific Pcx-knockout mice limitations: Genetic enzyme deletion is not a dietary biotin experiment. Cross-nutrient implications identify pathway dependence rather than a proven supplement response. exposure: Genetic deletion of hepatic pyruvate carboxylase evidence_span: {"source_cache": "artifacts/biotin-research/31006591.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e", "start_char": 0, "end_char": 1141, "text_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e"} [b7-p31006591] Pyruvate-Carboxylase-Mediated Anaplerosis Promotes Antioxidant Capacity by Sustaining TCA Cycle and Redox Metabolism in Liver. (2019). https://pubmed.ncbi.nlm.nih.gov/31006591/ DOI: 10.1016/j.cmet.2019.03.014
Complete structured claim and evidence
Liver-specific Pcx deletion depleted hepatic NADPH and worsened oxidative stress.
Liver-specific Pcx-null mouse genotype → Mouse liver NADPH pool source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/31006591.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e", "start_char": 0, "end_char": 1141, "text_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e"}
experimental_model
Liver-specific Pcx-knockout mice
exposure
Genetic deletion of hepatic pyruvate carboxylase
limitations
Genetic enzyme deletion is not a dietary biotin experiment. Cross-nutrient implications identify pathway dependence rather than a proven supplement response.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Mus musculus
plain_language
Failure of this carbon-supply step can affect the niacin-derived reducing-power pool.
primary_references
[b7-p31006591] Pyruvate-Carboxylase-Mediated Anaplerosis Promotes Antioxidant Capacity by Sustaining TCA Cycle and Redox Metabolism in Liver. (2019). https://pubmed.ncbi.nlm.nih.gov/31006591/ DOI: 10.1016/j.cmet.2019.03.014
tissue_or_cell_type
Liver and systemic metabolism
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 832–843
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Liver-specific Pcx-knockout mice · source_derived_draft · unverified_draft
### b7-pc-null-nadph Liver-specific Pcx deletion depleted hepatic NADPH and worsened oxidative stress. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Failure of this carbon-supply step can affect the niacin-derived reducing-power pool. organism: Mus musculus tissue_or_cell_type: Liver and systemic metabolism experimental_model: Liver-specific Pcx-knockout mice limitations: Genetic enzyme deletion is not a dietary biotin experiment. Cross-nutrient implications identify pathway dependence rather than a proven supplement response. exposure: Genetic deletion of hepatic pyruvate carboxylase evidence_span: {"source_cache": "artifacts/biotin-research/31006591.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e", "start_char": 0, "end_char": 1141, "text_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e"} [b7-p31006591] Pyruvate-Carboxylase-Mediated Anaplerosis Promotes Antioxidant Capacity by Sustaining TCA Cycle and Redox Metabolism in Liver. (2019). https://pubmed.ncbi.nlm.nih.gov/31006591/ DOI: 10.1016/j.cmet.2019.03.014
Complete structured claim and evidence
Liver-specific Pcx deletion depleted hepatic glutathione and was associated with greater oxidative stress and inflammation.
Liver-specific Pcx-null mouse genotype → Mouse liver glutathione pool source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/31006591.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e", "start_char": 0, "end_char": 1141, "text_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e"}
experimental_model
Liver-specific Pcx-knockout mice
exposure
Genetic deletion of hepatic pyruvate carboxylase
limitations
Genetic enzyme deletion is not a dietary biotin experiment. Cross-nutrient implications identify pathway dependence rather than a proven supplement response.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Mus musculus
plain_language
The consequences can reach antioxidant supply, not just fuel production.
primary_references
[b7-p31006591] Pyruvate-Carboxylase-Mediated Anaplerosis Promotes Antioxidant Capacity by Sustaining TCA Cycle and Redox Metabolism in Liver. (2019). https://pubmed.ncbi.nlm.nih.gov/31006591/ DOI: 10.1016/j.cmet.2019.03.014
tissue_or_cell_type
Liver and systemic metabolism
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 845–856
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Liver-specific Pcx-knockout mice · source_derived_draft · unverified_draft
### b7-pc-null-glutathione Liver-specific Pcx deletion depleted hepatic glutathione and was associated with greater oxidative stress and inflammation. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The consequences can reach antioxidant supply, not just fuel production. organism: Mus musculus tissue_or_cell_type: Liver and systemic metabolism experimental_model: Liver-specific Pcx-knockout mice limitations: Genetic enzyme deletion is not a dietary biotin experiment. Cross-nutrient implications identify pathway dependence rather than a proven supplement response. exposure: Genetic deletion of hepatic pyruvate carboxylase evidence_span: {"source_cache": "artifacts/biotin-research/31006591.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e", "start_char": 0, "end_char": 1141, "text_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e"} [b7-p31006591] Pyruvate-Carboxylase-Mediated Anaplerosis Promotes Antioxidant Capacity by Sustaining TCA Cycle and Redox Metabolism in Liver. (2019). https://pubmed.ncbi.nlm.nih.gov/31006591/ DOI: 10.1016/j.cmet.2019.03.014
Complete structured claim and evidence
Liver-specific Pcx deletion depleted aspartate and impaired urea-cycle function, with hyperammonemia.
Liver-specific Pcx-null mouse genotype → Mouse liver aspartate pool source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/31006591.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e", "start_char": 0, "end_char": 1141, "text_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e"}
experimental_model
Liver-specific Pcx-knockout mice
exposure
Genetic deletion of hepatic pyruvate carboxylase
limitations
Genetic enzyme deletion is not a dietary biotin experiment. Cross-nutrient implications identify pathway dependence rather than a proven supplement response.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Mus musculus
plain_language
Loss of carbon replenishment also constrained nitrogen disposal.
primary_references
[b7-p31006591] Pyruvate-Carboxylase-Mediated Anaplerosis Promotes Antioxidant Capacity by Sustaining TCA Cycle and Redox Metabolism in Liver. (2019). https://pubmed.ncbi.nlm.nih.gov/31006591/ DOI: 10.1016/j.cmet.2019.03.014
tissue_or_cell_type
Liver and systemic metabolism
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 858–869
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Liver-specific Pcx-knockout mice · source_derived_draft · unverified_draft
### b7-pc-null-aspartate Liver-specific Pcx deletion depleted aspartate and impaired urea-cycle function, with hyperammonemia. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of carbon replenishment also constrained nitrogen disposal. organism: Mus musculus tissue_or_cell_type: Liver and systemic metabolism experimental_model: Liver-specific Pcx-knockout mice limitations: Genetic enzyme deletion is not a dietary biotin experiment. Cross-nutrient implications identify pathway dependence rather than a proven supplement response. exposure: Genetic deletion of hepatic pyruvate carboxylase evidence_span: {"source_cache": "artifacts/biotin-research/31006591.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e", "start_char": 0, "end_char": 1141, "text_sha256": "0dcedbfac623863bd4ae86ed1bb97cef0ef56bd417bd0d49507ef47d16af7b4e"} [b7-p31006591] Pyruvate-Carboxylase-Mediated Anaplerosis Promotes Antioxidant Capacity by Sustaining TCA Cycle and Redox Metabolism in Liver. (2019). https://pubmed.ncbi.nlm.nih.gov/31006591/ DOI: 10.1016/j.cmet.2019.03.014
Complete structured claim and evidence
Genetic depletion of PC in human islets reduced glutathione and the GSH/GSSG ratio under nitrosative stress.
Human pyruvate carboxylase / PC → Human pancreatic-islet glutathione synthesis source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/34818536.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "48bcb3951c9b630862fdda839e0a54b80abe9e2cf2e79d0bfb7547e2af317523", "start_char": 35800, "end_char": 36138, "text_sha256": "b1dd7e5022ba64d19114d853d2f75c43e061cdca76e1938e95c19379e96c3933"}
experimental_model
Primary human-islet tracer metabolomics and PC knockdown under inflammatory/nitrosative stress
exposure
Glucose tracer, PC knockdown and nitric-oxide donor exposure
limitations
Genetic perturbation of PC in isolated islets is not dietary biotin depletion or evidence that biotin supplements raise glutathione in replete people.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
PC connects carbon metabolism to the cell’s ability to maintain glutathione.
primary_references
[b7-p34818536] Glucose metabolism and pyruvate carboxylase enhance glutathione synthesis and restrict oxidative stress in pancreatic islets. (2021). https://pubmed.ncbi.nlm.nih.gov/34818536/ DOI: 10.1016/j.celrep.2021.110037
tissue_or_cell_type
Primary human pancreatic islets
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 871–882
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human-islet tracer metabolomics and PC knockdown under inflammatory/nitrosative stress · source_derived_draft · unverified_draft
### b7-pc-islet-gsh Genetic depletion of PC in human islets reduced glutathione and the GSH/GSSG ratio under nitrosative stress. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: PC connects carbon metabolism to the cell’s ability to maintain glutathione. organism: Homo sapiens tissue_or_cell_type: Primary human pancreatic islets experimental_model: Primary human-islet tracer metabolomics and PC knockdown under inflammatory/nitrosative stress limitations: Genetic perturbation of PC in isolated islets is not dietary biotin depletion or evidence that biotin supplements raise glutathione in replete people. exposure: Glucose tracer, PC knockdown and nitric-oxide donor exposure evidence_span: {"source_cache": "artifacts/biotin-research/34818536.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "48bcb3951c9b630862fdda839e0a54b80abe9e2cf2e79d0bfb7547e2af317523", "start_char": 35800, "end_char": 36138, "text_sha256": "b1dd7e5022ba64d19114d853d2f75c43e061cdca76e1938e95c19379e96c3933"} [b7-p34818536] Glucose metabolism and pyruvate carboxylase enhance glutathione synthesis and restrict oxidative stress in pancreatic islets. (2021). https://pubmed.ncbi.nlm.nih.gov/34818536/ DOI: 10.1016/j.celrep.2021.110037
Complete structured claim and evidence
The experimental egg-white diet used avidin binding to reduce the availability of dietary biotin.
Chicken egg-white avidin → Biotin source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/12399279.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ce0c502ccaa9e8cdf49c65bd9a0e48146dbc4c6c082320ccdc05cbf750f61078", "start_char": 8594, "end_char": 9015, "text_sha256": "f006100b1360d2b0935240bebeef093e47caeb8016c955b5797ac0efb695ec2b"}
experimental_model
Experimental depletion/repletion in 11 healthy adults; leucine challenge in 5
exposure
28 days of egg-white diet followed by general diet with or without 80 micrograms supplemental biotin
limitations
An intentional undenatured egg-white diet is not ordinary cooked-egg intake. Small experimental cohorts do not establish a population-wide threshold.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Avidin in the experimental diet binds biotin before it can be used.
primary_references
[b7-p12399279] Indicators of marginal biotin deficiency and repletion in humans: validation of 3-hydroxyisovaleric acid excretion and a leucine challenge. (2002). https://pubmed.ncbi.nlm.nih.gov/12399279/ DOI: 10.1093/ajcn/76.5.1061
tissue_or_cell_type
Dietary exposure and urinary metabolites
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 884–895
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Experimental depletion/repletion in 11 healthy adults; leucine challenge in 5 · source_derived_draft · unverified_draft
### b7-avidin-sequestration The experimental egg-white diet used avidin binding to reduce the availability of dietary biotin. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Avidin in the experimental diet binds biotin before it can be used. organism: Homo sapiens tissue_or_cell_type: Dietary exposure and urinary metabolites experimental_model: Experimental depletion/repletion in 11 healthy adults; leucine challenge in 5 limitations: An intentional undenatured egg-white diet is not ordinary cooked-egg intake. Small experimental cohorts do not establish a population-wide threshold. exposure: 28 days of egg-white diet followed by general diet with or without 80 micrograms supplemental biotin evidence_span: {"source_cache": "artifacts/biotin-research/12399279.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ce0c502ccaa9e8cdf49c65bd9a0e48146dbc4c6c082320ccdc05cbf750f61078", "start_char": 8594, "end_char": 9015, "text_sha256": "f006100b1360d2b0935240bebeef093e47caeb8016c955b5797ac0efb695ec2b"} [b7-p12399279] Indicators of marginal biotin deficiency and repletion in humans: validation of 3-hydroxyisovaleric acid excretion and a leucine challenge. (2002). https://pubmed.ncbi.nlm.nih.gov/12399279/ DOI: 10.1093/ajcn/76.5.1061
Complete structured claim and evidence
Urinary 3-HIA increased during 28-day biotin depletion in 11 adults; biotin-status indicators normalized in most after one week on a general diet.
Biotin → Human urinary 3-hydroxyisovaleric acid excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/12399279.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "38158dd10cfc6528b65a3304fac58a5b5d8ec82e20673534b5bf6e9e79f14b09", "start_char": 0, "end_char": 1718, "text_sha256": "38158dd10cfc6528b65a3304fac58a5b5d8ec82e20673534b5bf6e9e79f14b09"}
experimental_model
Experimental depletion/repletion in 11 healthy adults; leucine challenge in 5
exposure
28 days of egg-white diet followed by general diet with or without 80 micrograms supplemental biotin
limitations
An intentional undenatured egg-white diet is not ordinary cooked-egg intake. Small experimental cohorts do not establish a population-wide threshold.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
A bottleneck in leucine breakdown became measurable before a universal clinical syndrome was required.
primary_references
[b7-p12399279] Indicators of marginal biotin deficiency and repletion in humans: validation of 3-hydroxyisovaleric acid excretion and a leucine challenge. (2002). https://pubmed.ncbi.nlm.nih.gov/12399279/ DOI: 10.1093/ajcn/76.5.1061
tissue_or_cell_type
Dietary exposure and urinary metabolites
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 897–908
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Experimental depletion/repletion in 11 healthy adults; leucine challenge in 5 · source_derived_draft · unverified_draft
### b7-depletion-3hia Urinary 3-HIA increased during 28-day biotin depletion in 11 adults; biotin-status indicators normalized in most after one week on a general diet. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A bottleneck in leucine breakdown became measurable before a universal clinical syndrome was required. organism: Homo sapiens tissue_or_cell_type: Dietary exposure and urinary metabolites experimental_model: Experimental depletion/repletion in 11 healthy adults; leucine challenge in 5 limitations: An intentional undenatured egg-white diet is not ordinary cooked-egg intake. Small experimental cohorts do not establish a population-wide threshold. exposure: 28 days of egg-white diet followed by general diet with or without 80 micrograms supplemental biotin evidence_span: {"source_cache": "artifacts/biotin-research/12399279.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "38158dd10cfc6528b65a3304fac58a5b5d8ec82e20673534b5bf6e9e79f14b09", "start_char": 0, "end_char": 1718, "text_sha256": "38158dd10cfc6528b65a3304fac58a5b5d8ec82e20673534b5bf6e9e79f14b09"} [b7-p12399279] Indicators of marginal biotin deficiency and repletion in humans: validation of 3-hydroxyisovaleric acid excretion and a leucine challenge. (2002). https://pubmed.ncbi.nlm.nih.gov/12399279/ DOI: 10.1093/ajcn/76.5.1061
Complete structured claim and evidence
Challenge-induced urinary 3-HIA rose more than twofold by day 14 in both biotin-depleted cohorts.
L-Leucine → Human urinary 3-hydroxyisovaleric acid excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/21918059.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5cf1d7e25ae7bdfeb2ac3225cee8e4e660723d5197fc057f63327b3ad9eb3aaf", "start_char": 0, "end_char": 1723, "text_sha256": "5cf1d7e25ae7bdfeb2ac3225cee8e4e660723d5197fc057f63327b3ad9eb3aaf"}
experimental_model
Leucine challenge during biotin depletion in two cohorts of 5 and 7 healthy adults
exposure
28-day egg-white depletion; weekly oral leucine challenge
limitations
The challenge was sensitive but not diagnostically superior to 24-hour urine measurements; no validated universal threshold follows.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Extra leucine made the impaired pathway easier to observe.
primary_references
[b7-p21918059] Urinary excretion of 3-hydroxyisovaleric acid and 3-hydroxyisovaleryl carnitine increases in response to a leucine challenge in marginally biotin-deficient humans. (2011). https://pubmed.ncbi.nlm.nih.gov/21918059/ DOI: 10.3945/jn.111.146126
tissue_or_cell_type
Urine
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 910–921
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Leucine challenge during biotin depletion in two cohorts of 5 and 7 healthy adults · source_derived_draft · unverified_draft
### b7-leucine-challenge-3hia Challenge-induced urinary 3-HIA rose more than twofold by day 14 in both biotin-depleted cohorts. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Extra leucine made the impaired pathway easier to observe. organism: Homo sapiens tissue_or_cell_type: Urine experimental_model: Leucine challenge during biotin depletion in two cohorts of 5 and 7 healthy adults limitations: The challenge was sensitive but not diagnostically superior to 24-hour urine measurements; no validated universal threshold follows. exposure: 28-day egg-white depletion; weekly oral leucine challenge evidence_span: {"source_cache": "artifacts/biotin-research/21918059.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5cf1d7e25ae7bdfeb2ac3225cee8e4e660723d5197fc057f63327b3ad9eb3aaf", "start_char": 0, "end_char": 1723, "text_sha256": "5cf1d7e25ae7bdfeb2ac3225cee8e4e660723d5197fc057f63327b3ad9eb3aaf"} [b7-p21918059] Urinary excretion of 3-hydroxyisovaleric acid and 3-hydroxyisovaleryl carnitine increases in response to a leucine challenge in marginally biotin-deficient humans. (2011). https://pubmed.ncbi.nlm.nih.gov/21918059/ DOI: 10.3945/jn.111.146126
Complete structured claim and evidence
Challenge-induced urinary 3-hydroxyisovalerylcarnitine rose more than twofold by day 14 in both biotin-depleted cohorts.
L-Leucine → Human urinary 3-hydroxyisovalerylcarnitine excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/21918059.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5cf1d7e25ae7bdfeb2ac3225cee8e4e660723d5197fc057f63327b3ad9eb3aaf", "start_char": 0, "end_char": 1723, "text_sha256": "5cf1d7e25ae7bdfeb2ac3225cee8e4e660723d5197fc057f63327b3ad9eb3aaf"}
experimental_model
Leucine challenge during biotin depletion in two cohorts of 5 and 7 healthy adults
exposure
28-day egg-white depletion; weekly oral leucine challenge
limitations
The challenge was sensitive but not diagnostically superior to 24-hour urine measurements; no validated universal threshold follows.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
The carnitine-linked side product also increased as biotin became limited.
primary_references
[b7-p21918059] Urinary excretion of 3-hydroxyisovaleric acid and 3-hydroxyisovaleryl carnitine increases in response to a leucine challenge in marginally biotin-deficient humans. (2011). https://pubmed.ncbi.nlm.nih.gov/21918059/ DOI: 10.3945/jn.111.146126
tissue_or_cell_type
Urine
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 923–934
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Leucine challenge during biotin depletion in two cohorts of 5 and 7 healthy adults · source_derived_draft · unverified_draft
### b7-leucine-challenge-c5oh Challenge-induced urinary 3-hydroxyisovalerylcarnitine rose more than twofold by day 14 in both biotin-depleted cohorts. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The carnitine-linked side product also increased as biotin became limited. organism: Homo sapiens tissue_or_cell_type: Urine experimental_model: Leucine challenge during biotin depletion in two cohorts of 5 and 7 healthy adults limitations: The challenge was sensitive but not diagnostically superior to 24-hour urine measurements; no validated universal threshold follows. exposure: 28-day egg-white depletion; weekly oral leucine challenge evidence_span: {"source_cache": "artifacts/biotin-research/21918059.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5cf1d7e25ae7bdfeb2ac3225cee8e4e660723d5197fc057f63327b3ad9eb3aaf", "start_char": 0, "end_char": 1723, "text_sha256": "5cf1d7e25ae7bdfeb2ac3225cee8e4e660723d5197fc057f63327b3ad9eb3aaf"} [b7-p21918059] Urinary excretion of 3-hydroxyisovaleric acid and 3-hydroxyisovaleryl carnitine increases in response to a leucine challenge in marginally biotin-deficient humans. (2011). https://pubmed.ncbi.nlm.nih.gov/21918059/ DOI: 10.3945/jn.111.146126
Complete structured claim and evidence
Plasma 3-hydroxyisovalerylcarnitine was above the study reference interval in 7 of 10 adults by day 14 and 9 of 10 by day 28 of depletion, then fell with repletion.
Biotin → Human plasma 3-hydroxyisovalerylcarnitine concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/20943794.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1351a960b61efdce767a72da73d9ad8755e52f935e98b9510b4f68c2d5b83c9a", "start_char": 0, "end_char": 1877, "text_sha256": "1351a960b61efdce767a72da73d9ad8755e52f935e98b9510b4f68c2d5b83c9a"}
experimental_model
Depletion/repletion in 10 healthy adults, 8 women
exposure
28 days of undenatured egg white, followed by repletion
limitations
The study-specific reference interval and 10 participants do not define a universally diagnostic blood cutoff.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
A blood marker tracked depletion in most, but not all, participants.
primary_references
[b7-p20943794] Plasma concentration of 3-hydroxyisovaleryl carnitine is an early and sensitive indicator of marginal biotin deficiency in humans. (2010). https://pubmed.ncbi.nlm.nih.gov/20943794/ DOI: 10.3945/ajcn.110.002543
tissue_or_cell_type
Plasma
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 936–947
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Depletion/repletion in 10 healthy adults, 8 women · source_derived_draft · unverified_draft
### b7-plasma-c5oh Plasma 3-hydroxyisovalerylcarnitine was above the study reference interval in 7 of 10 adults by day 14 and 9 of 10 by day 28 of depletion, then fell with repletion. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A blood marker tracked depletion in most, but not all, participants. organism: Homo sapiens tissue_or_cell_type: Plasma experimental_model: Depletion/repletion in 10 healthy adults, 8 women limitations: The study-specific reference interval and 10 participants do not define a universally diagnostic blood cutoff. exposure: 28 days of undenatured egg white, followed by repletion evidence_span: {"source_cache": "artifacts/biotin-research/20943794.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1351a960b61efdce767a72da73d9ad8755e52f935e98b9510b4f68c2d5b83c9a", "start_char": 0, "end_char": 1877, "text_sha256": "1351a960b61efdce767a72da73d9ad8755e52f935e98b9510b4f68c2d5b83c9a"} [b7-p20943794] Plasma concentration of 3-hydroxyisovaleryl carnitine is an early and sensitive indicator of marginal biotin deficiency in humans. (2010). https://pubmed.ncbi.nlm.nih.gov/20943794/ DOI: 10.3945/ajcn.110.002543
Complete structured claim and evidence
Biotin-deficient but carnitine-sufficient HepG2 cells had more than tenfold higher intracellular 3-hydroxyisovalerylcarnitine than doubly sufficient cells.
Biotin → HepG2 3-hydroxyisovalerylcarnitine pool source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/25527659.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4a368eb2fa2020bb1cabc99b31a3420870a8256886d5934d3d834c90b078238f", "start_char": 0, "end_char": 2372, "text_sha256": "4a368eb2fa2020bb1cabc99b31a3420870a8256886d5934d3d834c90b078238f"}
experimental_model
Two-factor biotin/carnitine depletion and carnitine repletion in human HepG2 cells
exposure
Separate and combined biotin and carnitine depletion
limitations
This is a cell-culture demonstration of marker masking; it does not validate a diagnostic correction formula in pregnancy or the general population.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
When carnitine is available, the biotin-related bottleneck produces a strong side-product signal.
primary_references
[b7-p25527659] In HepG2 cells, coexisting carnitine deficiency masks important indicators of marginal biotin deficiency. (2015). https://pubmed.ncbi.nlm.nih.gov/25527659/ DOI: 10.3945/jn.114.201343
tissue_or_cell_type
HepG2 hepatoma cells
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 949–960
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two-factor biotin/carnitine depletion and carnitine repletion in human HepG2 cells · source_derived_draft · unverified_draft
### b7-c5oh-biotin-low Biotin-deficient but carnitine-sufficient HepG2 cells had more than tenfold higher intracellular 3-hydroxyisovalerylcarnitine than doubly sufficient cells. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: When carnitine is available, the biotin-related bottleneck produces a strong side-product signal. organism: Homo sapiens tissue_or_cell_type: HepG2 hepatoma cells experimental_model: Two-factor biotin/carnitine depletion and carnitine repletion in human HepG2 cells limitations: This is a cell-culture demonstration of marker masking; it does not validate a diagnostic correction formula in pregnancy or the general population. exposure: Separate and combined biotin and carnitine depletion evidence_span: {"source_cache": "artifacts/biotin-research/25527659.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4a368eb2fa2020bb1cabc99b31a3420870a8256886d5934d3d834c90b078238f", "start_char": 0, "end_char": 2372, "text_sha256": "4a368eb2fa2020bb1cabc99b31a3420870a8256886d5934d3d834c90b078238f"} [b7-p25527659] In HepG2 cells, coexisting carnitine deficiency masks important indicators of marginal biotin deficiency. (2015). https://pubmed.ncbi.nlm.nih.gov/25527659/ DOI: 10.3945/jn.114.201343
Complete structured claim and evidence
Combined biotin and carnitine deficiency largely masked the increase in substrate-derived acylcarnitines observed with isolated biotin deficiency in HepG2 cells.
L-Carnitine → HepG2 3-hydroxyisovalerylcarnitine pool source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/25527659.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4a368eb2fa2020bb1cabc99b31a3420870a8256886d5934d3d834c90b078238f", "start_char": 0, "end_char": 2372, "text_sha256": "4a368eb2fa2020bb1cabc99b31a3420870a8256886d5934d3d834c90b078238f"}
experimental_model
Two-factor biotin/carnitine depletion and carnitine repletion in human HepG2 cells
exposure
Separate and combined biotin and carnitine depletion
limitations
This is a cell-culture demonstration of marker masking; it does not validate a diagnostic correction formula in pregnancy or the general population.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
A second shortage can hide the laboratory signature of the first.
primary_references
[b7-p25527659] In HepG2 cells, coexisting carnitine deficiency masks important indicators of marginal biotin deficiency. (2015). https://pubmed.ncbi.nlm.nih.gov/25527659/ DOI: 10.3945/jn.114.201343
tissue_or_cell_type
HepG2 hepatoma cells
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 962–973
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two-factor biotin/carnitine depletion and carnitine repletion in human HepG2 cells · source_derived_draft · unverified_draft
### b7-carnitine-hides-c5oh Combined biotin and carnitine deficiency largely masked the increase in substrate-derived acylcarnitines observed with isolated biotin deficiency in HepG2 cells. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second shortage can hide the laboratory signature of the first. organism: Homo sapiens tissue_or_cell_type: HepG2 hepatoma cells experimental_model: Two-factor biotin/carnitine depletion and carnitine repletion in human HepG2 cells limitations: This is a cell-culture demonstration of marker masking; it does not validate a diagnostic correction formula in pregnancy or the general population. exposure: Separate and combined biotin and carnitine depletion evidence_span: {"source_cache": "artifacts/biotin-research/25527659.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4a368eb2fa2020bb1cabc99b31a3420870a8256886d5934d3d834c90b078238f", "start_char": 0, "end_char": 2372, "text_sha256": "4a368eb2fa2020bb1cabc99b31a3420870a8256886d5934d3d834c90b078238f"} [b7-p25527659] In HepG2 cells, coexisting carnitine deficiency masks important indicators of marginal biotin deficiency. (2015). https://pubmed.ncbi.nlm.nih.gov/25527659/ DOI: 10.3945/jn.114.201343
Complete structured claim and evidence
Carnitine repletion of doubly deficient HepG2 cells increased acetylcarnitine, propionylcarnitine and 3-hydroxyisovalerylcarnitine each by more than 50-fold.
L-Carnitine → HepG2 acylcarnitine response to carnitine repletion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/25527659.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4a368eb2fa2020bb1cabc99b31a3420870a8256886d5934d3d834c90b078238f", "start_char": 0, "end_char": 2372, "text_sha256": "4a368eb2fa2020bb1cabc99b31a3420870a8256886d5934d3d834c90b078238f"}
experimental_model
Two-factor biotin/carnitine depletion and carnitine repletion in human HepG2 cells
exposure
Separate and combined biotin and carnitine depletion
limitations
This is a cell-culture demonstration of marker masking; it does not validate a diagnostic correction formula in pregnancy or the general population.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Restoring carnitine exposed the unresolved biotin-related bottleneck.
primary_references
[b7-p25527659] In HepG2 cells, coexisting carnitine deficiency masks important indicators of marginal biotin deficiency. (2015). https://pubmed.ncbi.nlm.nih.gov/25527659/ DOI: 10.3945/jn.114.201343
tissue_or_cell_type
HepG2 hepatoma cells
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 975–986
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two-factor biotin/carnitine depletion and carnitine repletion in human HepG2 cells · source_derived_draft · unverified_draft
### b7-carnitine-unmasking Carnitine repletion of doubly deficient HepG2 cells increased acetylcarnitine, propionylcarnitine and 3-hydroxyisovalerylcarnitine each by more than 50-fold. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring carnitine exposed the unresolved biotin-related bottleneck. organism: Homo sapiens tissue_or_cell_type: HepG2 hepatoma cells experimental_model: Two-factor biotin/carnitine depletion and carnitine repletion in human HepG2 cells limitations: This is a cell-culture demonstration of marker masking; it does not validate a diagnostic correction formula in pregnancy or the general population. exposure: Separate and combined biotin and carnitine depletion evidence_span: {"source_cache": "artifacts/biotin-research/25527659.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4a368eb2fa2020bb1cabc99b31a3420870a8256886d5934d3d834c90b078238f", "start_char": 0, "end_char": 2372, "text_sha256": "4a368eb2fa2020bb1cabc99b31a3420870a8256886d5934d3d834c90b078238f"} [b7-p25527659] In HepG2 cells, coexisting carnitine deficiency masks important indicators of marginal biotin deficiency. (2015). https://pubmed.ncbi.nlm.nih.gov/25527659/ DOI: 10.3945/jn.114.201343
Complete structured claim and evidence
At the controlled intake, pregnant women excreted 69% more 3-HIA than controls, while urinary 3-HIA-carnitine was 27% lower.
Biotin → Human urinary 3-hydroxyisovaleric acid excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/25122647.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6066b007a013c3c0c69336e7aba0e51baa39e3a24b6eb918cb4778e792376a9b", "start_char": 0, "end_char": 2354, "text_sha256": "6066b007a013c3c0c69336e7aba0e51baa39e3a24b6eb918cb4778e792376a9b"}
experimental_model
Controlled feeding: 26 pregnant, 28 lactating and 21 control women
exposure
57 micrograms dietary biotin per day for 10–12 weeks
limitations
Groups differed in reproductive state. Marker changes do not establish fetal outcomes, universal deficiency or a treatment dose.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Two related markers moved in opposite directions during pregnancy.
primary_references
[b7-p25122647] Pregnancy and lactation alter biomarkers of biotin metabolism in women consuming a controlled diet. (2014). https://pubmed.ncbi.nlm.nih.gov/25122647/ DOI: 10.3945/jn.114.194472
tissue_or_cell_type
Urine and plasma
trigger_kind
biomarker_context Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 988–999
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled feeding: 26 pregnant, 28 lactating and 21 control women · source_derived_draft · unverified_draft
### b7-pregnancy-3hia At the controlled intake, pregnant women excreted 69% more 3-HIA than controls, while urinary 3-HIA-carnitine was 27% lower. Condition category: biomarker_context nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Two related markers moved in opposite directions during pregnancy. organism: Homo sapiens tissue_or_cell_type: Urine and plasma experimental_model: Controlled feeding: 26 pregnant, 28 lactating and 21 control women limitations: Groups differed in reproductive state. Marker changes do not establish fetal outcomes, universal deficiency or a treatment dose. exposure: 57 micrograms dietary biotin per day for 10–12 weeks evidence_span: {"source_cache": "artifacts/biotin-research/25122647.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6066b007a013c3c0c69336e7aba0e51baa39e3a24b6eb918cb4778e792376a9b", "start_char": 0, "end_char": 2354, "text_sha256": "6066b007a013c3c0c69336e7aba0e51baa39e3a24b6eb918cb4778e792376a9b"} [b7-p25122647] Pregnancy and lactation alter biomarkers of biotin metabolism in women consuming a controlled diet. (2014). https://pubmed.ncbi.nlm.nih.gov/25122647/ DOI: 10.3945/jn.114.194472
Complete structured claim and evidence
Lactating women excreted 76% more bisnorbiotin than controls, while 3-HIA and 3-HIA-carnitine excretion were lower.
Biotin → Human urinary bisnorbiotin excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/25122647.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6066b007a013c3c0c69336e7aba0e51baa39e3a24b6eb918cb4778e792376a9b", "start_char": 0, "end_char": 2354, "text_sha256": "6066b007a013c3c0c69336e7aba0e51baa39e3a24b6eb918cb4778e792376a9b"}
experimental_model
Controlled feeding: 26 pregnant, 28 lactating and 21 control women
exposure
57 micrograms dietary biotin per day for 10–12 weeks
limitations
Groups differed in reproductive state. Marker changes do not establish fetal outcomes, universal deficiency or a treatment dose.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Biotin breakdown and leucine-derived markers can diverge during lactation.
primary_references
[b7-p25122647] Pregnancy and lactation alter biomarkers of biotin metabolism in women consuming a controlled diet. (2014). https://pubmed.ncbi.nlm.nih.gov/25122647/ DOI: 10.3945/jn.114.194472
tissue_or_cell_type
Urine and plasma
trigger_kind
biomarker_context Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1001–1012
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled feeding: 26 pregnant, 28 lactating and 21 control women · source_derived_draft · unverified_draft
### b7-lactation-bisnor Lactating women excreted 76% more bisnorbiotin than controls, while 3-HIA and 3-HIA-carnitine excretion were lower. Condition category: biomarker_context nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Biotin breakdown and leucine-derived markers can diverge during lactation. organism: Homo sapiens tissue_or_cell_type: Urine and plasma experimental_model: Controlled feeding: 26 pregnant, 28 lactating and 21 control women limitations: Groups differed in reproductive state. Marker changes do not establish fetal outcomes, universal deficiency or a treatment dose. exposure: 57 micrograms dietary biotin per day for 10–12 weeks evidence_span: {"source_cache": "artifacts/biotin-research/25122647.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6066b007a013c3c0c69336e7aba0e51baa39e3a24b6eb918cb4778e792376a9b", "start_char": 0, "end_char": 2354, "text_sha256": "6066b007a013c3c0c69336e7aba0e51baa39e3a24b6eb918cb4778e792376a9b"} [b7-p25122647] Pregnancy and lactation alter biomarkers of biotin metabolism in women consuming a controlled diet. (2014). https://pubmed.ncbi.nlm.nih.gov/25122647/ DOI: 10.3945/jn.114.194472
Complete structured claim and evidence
Maternal biotin deprivation caused severe malformations in mice, no observed fetal malformations in rats, and high embryonic lethality in hamsters.
Biotin → Rodent fetal malformations during maternal biotin deprivation source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/2918398.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a278d26fdd2c475c22b9b7f8cdeb6e11720872342805cab9ee6886ede7380bc3", "start_char": 0, "end_char": 812, "text_sha256": "a278d26fdd2c475c22b9b7f8cdeb6e11720872342805cab9ee6886ede7380bc3"}
experimental_model
Maternal biotin-deprivation comparison across mice, rats and Syrian hamsters
exposure
Biotin deprivation during gestation
limitations
Strong species and strain differences; this does not prove biotin deficiency causes the same malformations in humans.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Mus musculus; Rattus norvegicus; Mesocricetus auratus
plain_language
Animal findings establish vulnerability while also showing why direct human extrapolation is unsafe.
primary_references
[b7-p2918398] Species and strain differences in teratogenic effects of biotin deficiency in rodents. (1989). https://pubmed.ncbi.nlm.nih.gov/2918398/ DOI: 10.1093/jn/119.2.255
tissue_or_cell_type
Maternal-fetal systems
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1014–1025
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Maternal biotin-deprivation comparison across mice, rats and Syrian hamsters · source_derived_draft · unverified_draft
### b7-rodent-teratogenesis Maternal biotin deprivation caused severe malformations in mice, no observed fetal malformations in rats, and high embryonic lethality in hamsters. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Animal findings establish vulnerability while also showing why direct human extrapolation is unsafe. organism: Mus musculus; Rattus norvegicus; Mesocricetus auratus tissue_or_cell_type: Maternal-fetal systems experimental_model: Maternal biotin-deprivation comparison across mice, rats and Syrian hamsters limitations: Strong species and strain differences; this does not prove biotin deficiency causes the same malformations in humans. exposure: Biotin deprivation during gestation evidence_span: {"source_cache": "artifacts/biotin-research/2918398.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a278d26fdd2c475c22b9b7f8cdeb6e11720872342805cab9ee6886ede7380bc3", "start_char": 0, "end_char": 812, "text_sha256": "a278d26fdd2c475c22b9b7f8cdeb6e11720872342805cab9ee6886ede7380bc3"} [b7-p2918398] Species and strain differences in teratogenic effects of biotin deficiency in rodents. (1989). https://pubmed.ncbi.nlm.nih.gov/2918398/ DOI: 10.1093/jn/119.2.255
Complete structured claim and evidence
In the 88-person MCC-deficiency series, 57% were asymptomatic; 12 had acute metabolic decompensations, and genotype or biochemical phenotype did not reliably predict the course.
Human 3-methylcrotonyl-CoA carboxylase complex → Clinical course of human isolated MCC deficiency source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/22642865.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f0c40118afe81e9b597d2d2cbe6a785c2b96a4dbd7f4dcb634230070c61865ee", "start_char": 0, "end_char": 1384, "text_sha256": "f0c40118afe81e9b597d2d2cbe6a785c2b96a4dbd7f4dcb634230070c61865ee"}
experimental_model
Retrospective clinical, biochemical and molecular study of 88 MCC-deficient individuals
exposure
MCCC1/MCCC2 defects; mixed newborn screening and clinical ascertainment
limitations
Ascertainment bias and incomplete penetrance limit predictions. This is an isolated inherited enzyme defect, not biotin intake deficiency.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
A striking biochemical marker does not determine how ill a person will be.
primary_references
[b7-p22642865] 3-methylcrotonyl-CoA carboxylase deficiency: clinical, biochemical, enzymatic and molecular studies in 88 individuals. (2012). https://pubmed.ncbi.nlm.nih.gov/22642865/ DOI: 10.1186/1750-1172-7-31
tissue_or_cell_type
Clinical and biochemical phenotype
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1027–1038
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Retrospective clinical, biochemical and molecular study of 88 MCC-deficient individuals · source_derived_draft · unverified_draft
### b7-mcc-genetic-variability In the 88-person MCC-deficiency series, 57% were asymptomatic; 12 had acute metabolic decompensations, and genotype or biochemical phenotype did not reliably predict the course. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A striking biochemical marker does not determine how ill a person will be. organism: Homo sapiens tissue_or_cell_type: Clinical and biochemical phenotype experimental_model: Retrospective clinical, biochemical and molecular study of 88 MCC-deficient individuals limitations: Ascertainment bias and incomplete penetrance limit predictions. This is an isolated inherited enzyme defect, not biotin intake deficiency. exposure: MCCC1/MCCC2 defects; mixed newborn screening and clinical ascertainment evidence_span: {"source_cache": "artifacts/biotin-research/22642865.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f0c40118afe81e9b597d2d2cbe6a785c2b96a4dbd7f4dcb634230070c61865ee", "start_char": 0, "end_char": 1384, "text_sha256": "f0c40118afe81e9b597d2d2cbe6a785c2b96a4dbd7f4dcb634230070c61865ee"} [b7-p22642865] 3-methylcrotonyl-CoA carboxylase deficiency: clinical, biochemical, enzymatic and molecular studies in 88 individuals. (2012). https://pubmed.ncbi.nlm.nih.gov/22642865/ DOI: 10.1186/1750-1172-7-31
Complete structured claim and evidence
Premature twins on vitamin-limited parenteral nutrition developed severe illness associated with B2/B7 deficiency; the surviving twin improved after both vitamins were supplied.
Biotin → Clinical findings in combined B2 and B7 deficiency in preterm infants source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/37085971.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "981b9e33d62aaeda20905c76b8da3a96b2d5d8184a707beed7de5f66498974b5", "start_char": 0, "end_char": 1081, "text_sha256": "981b9e33d62aaeda20905c76b8da3a96b2d5d8184a707beed7de5f66498974b5"}
experimental_model
Case report of extremely premature twins during a parenteral multivitamin shortage
exposure
Combined B2 and B7 deficiency on prolonged parenteral nutrition
limitations
Two highly vulnerable infants and multiple concurrent problems; improvement after combined treatment cannot be attributed to biotin alone.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
The case illustrates interacting shortages, without identifying which vitamin caused each finding.
primary_references
[b7-p37085971] Twin Premature Infants With Riboflavin and Biotin Deficiency Presenting With Refractory Lactic Acidosis, Rash, and Multiorgan Failure During Prolonged Parenteral Nutrition. (2023). https://pubmed.ncbi.nlm.nih.gov/37085971/ DOI: 10.1177/23247096231168111
tissue_or_cell_type
Multisystem neonatal illness
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1040–1051
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Case report of extremely premature twins during a parenteral multivitamin shortage · source_derived_draft · unverified_draft
### b7-combined-b2-b7 Premature twins on vitamin-limited parenteral nutrition developed severe illness associated with B2/B7 deficiency; the surviving twin improved after both vitamins were supplied. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The case illustrates interacting shortages, without identifying which vitamin caused each finding. organism: Homo sapiens tissue_or_cell_type: Multisystem neonatal illness experimental_model: Case report of extremely premature twins during a parenteral multivitamin shortage limitations: Two highly vulnerable infants and multiple concurrent problems; improvement after combined treatment cannot be attributed to biotin alone. exposure: Combined B2 and B7 deficiency on prolonged parenteral nutrition evidence_span: {"source_cache": "artifacts/biotin-research/37085971.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "981b9e33d62aaeda20905c76b8da3a96b2d5d8184a707beed7de5f66498974b5", "start_char": 0, "end_char": 1081, "text_sha256": "981b9e33d62aaeda20905c76b8da3a96b2d5d8184a707beed7de5f66498974b5"} [b7-p37085971] Twin Premature Infants With Riboflavin and Biotin Deficiency Presenting With Refractory Lactic Acidosis, Rash, and Multiorgan Failure During Prolonged Parenteral Nutrition. (2023). https://pubmed.ncbi.nlm.nih.gov/37085971/ DOI: 10.1177/23247096231168111
Complete structured claim and evidence
Biotin-deficient human CD4 T cells secreted more IFN-gamma after anti-CD3/CD28 stimulation.
Biotin → T-cell interferon gamma production source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/29531163.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f", "start_char": 0, "end_char": 1720, "text_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f"}
experimental_model
Anti-CD3/CD28-stimulated human CD4 T cells in biotin-deficient culture; separate mouse validation
exposure
Defined biotin deficiency and signaling experiments
limitations
Cell-culture inflammation does not show that extra biotin treats autoimmune disease in replete people.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Activated T cells released more of one inflammatory signal.
primary_references
[b7-p29531163] Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29531163/ DOI: 10.4049/jimmunol.1701200
tissue_or_cell_type
Activated CD4 T cells
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1053–1064
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Anti-CD3/CD28-stimulated human CD4 T cells in biotin-deficient culture; separate mouse validation · source_derived_draft · unverified_draft
### b7-immune-ifng Biotin-deficient human CD4 T cells secreted more IFN-gamma after anti-CD3/CD28 stimulation. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Activated T cells released more of one inflammatory signal. organism: Homo sapiens tissue_or_cell_type: Activated CD4 T cells experimental_model: Anti-CD3/CD28-stimulated human CD4 T cells in biotin-deficient culture; separate mouse validation limitations: Cell-culture inflammation does not show that extra biotin treats autoimmune disease in replete people. exposure: Defined biotin deficiency and signaling experiments evidence_span: {"source_cache": "artifacts/biotin-research/29531163.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f", "start_char": 0, "end_char": 1720, "text_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f"} [b7-p29531163] Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29531163/ DOI: 10.4049/jimmunol.1701200
Complete structured claim and evidence
Biotin-deficient human CD4 T cells secreted more TNF after anti-CD3/CD28 stimulation.
Biotin → T-cell tumor necrosis factor production source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/29531163.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f", "start_char": 0, "end_char": 1720, "text_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f"}
experimental_model
Anti-CD3/CD28-stimulated human CD4 T cells in biotin-deficient culture; separate mouse validation
exposure
Defined biotin deficiency and signaling experiments
limitations
Cell-culture inflammation does not show that extra biotin treats autoimmune disease in replete people.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
A second inflammatory signal also increased.
primary_references
[b7-p29531163] Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29531163/ DOI: 10.4049/jimmunol.1701200
tissue_or_cell_type
Activated CD4 T cells
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1066–1077
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Anti-CD3/CD28-stimulated human CD4 T cells in biotin-deficient culture; separate mouse validation · source_derived_draft · unverified_draft
### b7-immune-tnf Biotin-deficient human CD4 T cells secreted more TNF after anti-CD3/CD28 stimulation. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second inflammatory signal also increased. organism: Homo sapiens tissue_or_cell_type: Activated CD4 T cells experimental_model: Anti-CD3/CD28-stimulated human CD4 T cells in biotin-deficient culture; separate mouse validation limitations: Cell-culture inflammation does not show that extra biotin treats autoimmune disease in replete people. exposure: Defined biotin deficiency and signaling experiments evidence_span: {"source_cache": "artifacts/biotin-research/29531163.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f", "start_char": 0, "end_char": 1720, "text_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f"} [b7-p29531163] Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29531163/ DOI: 10.4049/jimmunol.1701200
Complete structured claim and evidence
Biotin-deficient human CD4 T cells secreted more IL-17 after anti-CD3/CD28 stimulation.
Biotin → Human CD4 T-cell IL-17 secretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/29531163.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f", "start_char": 0, "end_char": 1720, "text_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f"}
experimental_model
Anti-CD3/CD28-stimulated human CD4 T cells in biotin-deficient culture; separate mouse validation
exposure
Defined biotin deficiency and signaling experiments
limitations
Cell-culture inflammation does not show that extra biotin treats autoimmune disease in replete people.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
The response also shifted toward an IL-17-associated inflammatory pattern.
primary_references
[b7-p29531163] Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29531163/ DOI: 10.4049/jimmunol.1701200
tissue_or_cell_type
Activated CD4 T cells
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1079–1090
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Anti-CD3/CD28-stimulated human CD4 T cells in biotin-deficient culture; separate mouse validation · source_derived_draft · unverified_draft
### b7-immune-il17 Biotin-deficient human CD4 T cells secreted more IL-17 after anti-CD3/CD28 stimulation. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response also shifted toward an IL-17-associated inflammatory pattern. organism: Homo sapiens tissue_or_cell_type: Activated CD4 T cells experimental_model: Anti-CD3/CD28-stimulated human CD4 T cells in biotin-deficient culture; separate mouse validation limitations: Cell-culture inflammation does not show that extra biotin treats autoimmune disease in replete people. exposure: Defined biotin deficiency and signaling experiments evidence_span: {"source_cache": "artifacts/biotin-research/29531163.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f", "start_char": 0, "end_char": 1720, "text_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f"} [b7-p29531163] Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29531163/ DOI: 10.4049/jimmunol.1701200
Complete structured claim and evidence
The study linked the heightened inflammatory response of biotin-deficient human CD4 T cells to enhanced mTOR-pathway activation.
Biotin → Human CD4 T-cell mTOR pathway activation source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/29531163.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f", "start_char": 0, "end_char": 1720, "text_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f"}
experimental_model
Anti-CD3/CD28-stimulated human CD4 T cells in biotin-deficient culture; separate mouse validation
exposure
Defined biotin deficiency and signaling experiments
limitations
Cell-culture inflammation does not show that extra biotin treats autoimmune disease in replete people.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Changes in metabolic signaling accompanied the altered immune response.
primary_references
[b7-p29531163] Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29531163/ DOI: 10.4049/jimmunol.1701200
tissue_or_cell_type
Activated CD4 T cells
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1092–1103
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Anti-CD3/CD28-stimulated human CD4 T cells in biotin-deficient culture; separate mouse validation · source_derived_draft · unverified_draft
### b7-immune-mtor The study linked the heightened inflammatory response of biotin-deficient human CD4 T cells to enhanced mTOR-pathway activation. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Changes in metabolic signaling accompanied the altered immune response. organism: Homo sapiens tissue_or_cell_type: Activated CD4 T cells experimental_model: Anti-CD3/CD28-stimulated human CD4 T cells in biotin-deficient culture; separate mouse validation limitations: Cell-culture inflammation does not show that extra biotin treats autoimmune disease in replete people. exposure: Defined biotin deficiency and signaling experiments evidence_span: {"source_cache": "artifacts/biotin-research/29531163.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f", "start_char": 0, "end_char": 1720, "text_sha256": "64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f"} [b7-p29531163] Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29531163/ DOI: 10.4049/jimmunol.1701200
Complete structured claim and evidence
LPS reduced the cell-surface fraction of SMVT in NCM460 cells without reducing total SMVT protein or RNA.
Lipopolysaccharide → Human colonic epithelial cell-surface SMVT abundance source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/28052864.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f27f27a7730837eff6529a7eccf67b3587df28af01ac0507d1b692410483703", "start_char": 0, "end_char": 1549, "text_sha256": "2f27f27a7730837eff6529a7eccf67b3587df28af01ac0507d1b692410483703"}
experimental_model
LPS exposure of human NCM460 cells with separate mouse experiments
exposure
LPS, CK2 inhibitors and SMVT Thr78Ala mutation
limitations
CK2 involvement is supported experimentally but the full causal sequence remains qualified; whole-body human deficiency was not measured.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Total transporter abundance can look normal while functional surface availability falls.
primary_references
[b7-p28052864] Lipopolysaccharide inhibits colonic biotin uptake via interference with membrane expression of its transporter: a role for a casein kinase 2-mediated pathway. (2017). https://pubmed.ncbi.nlm.nih.gov/28052864/ DOI: 10.1152/ajpcell.00300.2016
tissue_or_cell_type
Colonic epithelial NCM460 cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1105–1116
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · LPS exposure of human NCM460 cells with separate mouse experiments · source_derived_draft · unverified_draft
### b7-lps-surface LPS reduced the cell-surface fraction of SMVT in NCM460 cells without reducing total SMVT protein or RNA. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Total transporter abundance can look normal while functional surface availability falls. organism: Homo sapiens tissue_or_cell_type: Colonic epithelial NCM460 cells experimental_model: LPS exposure of human NCM460 cells with separate mouse experiments limitations: CK2 involvement is supported experimentally but the full causal sequence remains qualified; whole-body human deficiency was not measured. exposure: LPS, CK2 inhibitors and SMVT Thr78Ala mutation evidence_span: {"source_cache": "artifacts/biotin-research/28052864.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f27f27a7730837eff6529a7eccf67b3587df28af01ac0507d1b692410483703", "start_char": 0, "end_char": 1549, "text_sha256": "2f27f27a7730837eff6529a7eccf67b3587df28af01ac0507d1b692410483703"} [b7-p28052864] Lipopolysaccharide inhibits colonic biotin uptake via interference with membrane expression of its transporter: a role for a casein kinase 2-mediated pathway. (2017). https://pubmed.ncbi.nlm.nih.gov/28052864/ DOI: 10.1152/ajpcell.00300.2016
Complete structured claim and evidence
LPS reduced carrier-mediated biotin uptake in NCM460 cells; CK2 inhibition and a putative CK2-site SMVT mutant supported a CK2-related trafficking mechanism.
Lipopolysaccharide → Human colonic epithelial biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/28052864.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f27f27a7730837eff6529a7eccf67b3587df28af01ac0507d1b692410483703", "start_char": 0, "end_char": 1549, "text_sha256": "2f27f27a7730837eff6529a7eccf67b3587df28af01ac0507d1b692410483703"}
experimental_model
LPS exposure of human NCM460 cells with separate mouse experiments
exposure
LPS, CK2 inhibitors and SMVT Thr78Ala mutation
limitations
CK2 involvement is supported experimentally but the full causal sequence remains qualified; whole-body human deficiency was not measured.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Inflammatory exposure interfered with biotin entry in this model.
primary_references
[b7-p28052864] Lipopolysaccharide inhibits colonic biotin uptake via interference with membrane expression of its transporter: a role for a casein kinase 2-mediated pathway. (2017). https://pubmed.ncbi.nlm.nih.gov/28052864/ DOI: 10.1152/ajpcell.00300.2016
tissue_or_cell_type
Colonic epithelial NCM460 cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1118–1129
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · LPS exposure of human NCM460 cells with separate mouse experiments · source_derived_draft · unverified_draft
### b7-lps-uptake LPS reduced carrier-mediated biotin uptake in NCM460 cells; CK2 inhibition and a putative CK2-site SMVT mutant supported a CK2-related trafficking mechanism. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Inflammatory exposure interfered with biotin entry in this model. organism: Homo sapiens tissue_or_cell_type: Colonic epithelial NCM460 cells experimental_model: LPS exposure of human NCM460 cells with separate mouse experiments limitations: CK2 involvement is supported experimentally but the full causal sequence remains qualified; whole-body human deficiency was not measured. exposure: LPS, CK2 inhibitors and SMVT Thr78Ala mutation evidence_span: {"source_cache": "artifacts/biotin-research/28052864.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f27f27a7730837eff6529a7eccf67b3587df28af01ac0507d1b692410483703", "start_char": 0, "end_char": 1549, "text_sha256": "2f27f27a7730837eff6529a7eccf67b3587df28af01ac0507d1b692410483703"} [b7-p28052864] Lipopolysaccharide inhibits colonic biotin uptake via interference with membrane expression of its transporter: a role for a casein kinase 2-mediated pathway. (2017). https://pubmed.ncbi.nlm.nih.gov/28052864/ DOI: 10.1152/ajpcell.00300.2016
Complete structured claim and evidence
Vancomycin-associated L. murinus expansion consumed residual gut biotin in the mouse experiments.
Lactobacillus murinus → Intestinal luminal biotin availability source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/28813664.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a672505b5121e4c99b21436c378624a7a8eca2576090dba1f59b4a989182e7a9", "start_char": 0, "end_char": 1065, "text_sha256": "a672505b5121e4c99b21436c378624a7a8eca2576090dba1f59b4a989182e7a9"}
experimental_model
SPF and gnotobiotic mouse experiments with diet, vancomycin and Lactobacillus murinus
exposure
Biotin-deprived diet plus microbiota manipulation
limitations
Mouse experimental ecology does not diagnose the cause of human alopecia or justify targeting a bacterial species in people.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Mus musculus
plain_language
A microbe can use the nutrient instead of supplying it.
primary_references
[b7-p28813664] Intestinal Dysbiosis and Biotin Deprivation Induce Alopecia through Overgrowth of Lactobacillus murinus in Mice. (2017). https://pubmed.ncbi.nlm.nih.gov/28813664/ DOI: 10.1016/j.celrep.2017.07.057
tissue_or_cell_type
Gut microbiota and skin
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1131–1142
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SPF and gnotobiotic mouse experiments with diet, vancomycin and Lactobacillus murinus · source_derived_draft · unverified_draft
### b7-murinus-biotin Vancomycin-associated L. murinus expansion consumed residual gut biotin in the mouse experiments. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A microbe can use the nutrient instead of supplying it. organism: Mus musculus tissue_or_cell_type: Gut microbiota and skin experimental_model: SPF and gnotobiotic mouse experiments with diet, vancomycin and Lactobacillus murinus limitations: Mouse experimental ecology does not diagnose the cause of human alopecia or justify targeting a bacterial species in people. exposure: Biotin-deprived diet plus microbiota manipulation evidence_span: {"source_cache": "artifacts/biotin-research/28813664.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a672505b5121e4c99b21436c378624a7a8eca2576090dba1f59b4a989182e7a9", "start_char": 0, "end_char": 1065, "text_sha256": "a672505b5121e4c99b21436c378624a7a8eca2576090dba1f59b4a989182e7a9"} [b7-p28813664] Intestinal Dysbiosis and Biotin Deprivation Induce Alopecia through Overgrowth of Lactobacillus murinus in Mice. (2017). https://pubmed.ncbi.nlm.nih.gov/28813664/ DOI: 10.1016/j.celrep.2017.07.057
Complete structured claim and evidence
Biotin restored hair in SPF mice with established alopecia after combined dietary deprivation and vancomycin-associated dysbiosis.
Biotin → Mouse alopecia under biotin deprivation and dysbiosis source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/28813664.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a672505b5121e4c99b21436c378624a7a8eca2576090dba1f59b4a989182e7a9", "start_char": 0, "end_char": 1065, "text_sha256": "a672505b5121e4c99b21436c378624a7a8eca2576090dba1f59b4a989182e7a9"}
experimental_model
SPF and gnotobiotic mouse experiments with diet, vancomycin and Lactobacillus murinus
exposure
Biotin-deprived diet plus microbiota manipulation
limitations
Mouse experimental ecology does not diagnose the cause of human alopecia or justify targeting a bacterial species in people.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Mus musculus
plain_language
Correction helped in this experimentally induced mouse deficiency state.
primary_references
[b7-p28813664] Intestinal Dysbiosis and Biotin Deprivation Induce Alopecia through Overgrowth of Lactobacillus murinus in Mice. (2017). https://pubmed.ncbi.nlm.nih.gov/28813664/ DOI: 10.1016/j.celrep.2017.07.057
tissue_or_cell_type
Gut microbiota and skin
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1144–1155
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SPF and gnotobiotic mouse experiments with diet, vancomycin and Lactobacillus murinus · source_derived_draft · unverified_draft
### b7-microbiome-alopecia Biotin restored hair in SPF mice with established alopecia after combined dietary deprivation and vancomycin-associated dysbiosis. Condition category: nutrient_deficiency nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Correction helped in this experimentally induced mouse deficiency state. organism: Mus musculus tissue_or_cell_type: Gut microbiota and skin experimental_model: SPF and gnotobiotic mouse experiments with diet, vancomycin and Lactobacillus murinus limitations: Mouse experimental ecology does not diagnose the cause of human alopecia or justify targeting a bacterial species in people. exposure: Biotin-deprived diet plus microbiota manipulation evidence_span: {"source_cache": "artifacts/biotin-research/28813664.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a672505b5121e4c99b21436c378624a7a8eca2576090dba1f59b4a989182e7a9", "start_char": 0, "end_char": 1065, "text_sha256": "a672505b5121e4c99b21436c378624a7a8eca2576090dba1f59b4a989182e7a9"} [b7-p28813664] Intestinal Dysbiosis and Biotin Deprivation Induce Alopecia through Overgrowth of Lactobacillus murinus in Mice. (2017). https://pubmed.ncbi.nlm.nih.gov/28813664/ DOI: 10.1016/j.celrep.2017.07.057
Complete structured claim and evidence
The 2004 study identified H4 K8/K12 as candidate biotinylation sites in peptide assays and reported K12-biotinylated H4 immunoreactivity in human nuclear extracts.
Biotin → Human histone H4 K12 biotinylation reported in selected assays source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/15153116.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a3297d283f8a3980a77f1ba1d53f326fb32ee3971c76bda71ef9ba235fb53965", "start_char": 0, "end_char": 1762, "text_sha256": "a3297d283f8a3980a77f1ba1d53f326fb32ee3971c76bda71ef9ba235fb53965"}
experimental_model
Synthetic human histone H4 peptide biotinylation and human nuclear-extract immunodetection
exposure
Biotinidase incubation, residue substitutions and antibody/streptavidin detection
limitations
Peptide reactions and immunoreactivity do not establish abundant endogenous histone biotinylation; later assay-method work explicitly challenges this interpretation.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Early experiments proposed that biotin could also mark histones.
primary_references
[b7-p15153116] K8 and K12 are biotinylated in human histone H4. (2004). https://pubmed.ncbi.nlm.nih.gov/15153116/ DOI: 10.1111/j.1432-1033.2004.04167.x
tissue_or_cell_type
Synthetic H4 peptides and human cell extracts
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1157–1168
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Synthetic human histone H4 peptide biotinylation and human nuclear-extract immunodetection · source_derived_draft · unverified_draft
### b7-histone-h4-report The 2004 study identified H4 K8/K12 as candidate biotinylation sites in peptide assays and reported K12-biotinylated H4 immunoreactivity in human nuclear extracts. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Early experiments proposed that biotin could also mark histones. organism: Homo sapiens tissue_or_cell_type: Synthetic H4 peptides and human cell extracts experimental_model: Synthetic human histone H4 peptide biotinylation and human nuclear-extract immunodetection limitations: Peptide reactions and immunoreactivity do not establish abundant endogenous histone biotinylation; later assay-method work explicitly challenges this interpretation. exposure: Biotinidase incubation, residue substitutions and antibody/streptavidin detection evidence_span: {"source_cache": "artifacts/biotin-research/15153116.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a3297d283f8a3980a77f1ba1d53f326fb32ee3971c76bda71ef9ba235fb53965", "start_char": 0, "end_char": 1762, "text_sha256": "a3297d283f8a3980a77f1ba1d53f326fb32ee3971c76bda71ef9ba235fb53965"} [b7-p15153116] K8 and K12 are biotinylated in human histone H4. (2004). https://pubmed.ncbi.nlm.nih.gov/15153116/ DOI: 10.1111/j.1432-1033.2004.04167.x
Complete structured claim and evidence
The 2008 assay study found biotin-independent streptavidin binding to histones and detected radiolabeled biotin on carboxylases but not histones.
Streptavidin → Streptavidin binding in histone detection assays source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/17920026.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4b20857841bd32babc7962b138c4e56b6502a92d3bd6443e83fc0be32308e26d", "start_char": 0, "end_char": 1357, "text_sha256": "4b20857841bd32babc7962b138c4e56b6502a92d3bd6443e83fc0be32308e26d"}
experimental_model
Cell-culture biotin depletion, streptavidin controls and radiolabeled-biotin incorporation
exposure
Assay-method comparison
limitations
Failure to detect is an upper bound, not proof of zero; the stated less-than-0.03% bound is compatible numerically with the later less-than-0.001% estimate.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Cultured cells as specified in the primary paper
plain_language
A histone band can arise from the detection reagent rather than a biotin attachment.
primary_references
[b7-p17920026] Artifactual detection of biotin on histones by streptavidin. (2008). https://pubmed.ncbi.nlm.nih.gov/17920026/ DOI: 10.1016/j.ab.2007.09.003
tissue_or_cell_type
Histones and carboxylases
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1170–1181
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-culture biotin depletion, streptavidin controls and radiolabeled-biotin incorporation · source_derived_draft · unverified_draft
### b7-histone-artifact The 2008 assay study found biotin-independent streptavidin binding to histones and detected radiolabeled biotin on carboxylases but not histones. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A histone band can arise from the detection reagent rather than a biotin attachment. organism: Cultured cells as specified in the primary paper tissue_or_cell_type: Histones and carboxylases experimental_model: Cell-culture biotin depletion, streptavidin controls and radiolabeled-biotin incorporation limitations: Failure to detect is an upper bound, not proof of zero; the stated less-than-0.03% bound is compatible numerically with the later less-than-0.001% estimate. exposure: Assay-method comparison evidence_span: {"source_cache": "artifacts/biotin-research/17920026.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4b20857841bd32babc7962b138c4e56b6502a92d3bd6443e83fc0be32308e26d", "start_char": 0, "end_char": 1357, "text_sha256": "4b20857841bd32babc7962b138c4e56b6502a92d3bd6443e83fc0be32308e26d"} [b7-p17920026] Artifactual detection of biotin on histones by streptavidin. (2008). https://pubmed.ncbi.nlm.nih.gov/17920026/ DOI: 10.1016/j.ab.2007.09.003
Complete structured claim and evidence
The 2011 study reported natural biotinylation of less than 0.001% of human H3/H4 and argued for rare modification rather than a universal assay artifact.
Biotin → Detection of biotin on human histones source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/21930408.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "51af2341c7be0cb58c57e09784ebb8daabdd98cc93f04be52bb7b04b496e0b91", "start_char": 0, "end_char": 1318, "text_sha256": "51af2341c7be0cb58c57e09784ebb8daabdd98cc93f04be52bb7b04b496e0b91"}
experimental_model
Multiple antibody, radiotracer and cell-line comparisons of human histone biotinylation
exposure
Assay comparisons responding to artifact criticism
limitations
Authors estimated extremely low abundance and proposed HLCS chromatin scaffolding as a working model; nutritional epigenetic benefit was not demonstrated.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Later work defended a very rare mark while questioning whether that tiny amount explains biological effects.
primary_references
[b7-p21930408] Biotinylation is a natural, albeit rare, modification of human histones. (2011). https://pubmed.ncbi.nlm.nih.gov/21930408/ DOI: 10.1016/j.ymgme.2011.08.030
tissue_or_cell_type
Human histones H3/H4 in cultured cells
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1183–1194
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Multiple antibody, radiotracer and cell-line comparisons of human histone biotinylation · source_derived_draft · unverified_draft
### b7-histone-rare-report The 2011 study reported natural biotinylation of less than 0.001% of human H3/H4 and argued for rare modification rather than a universal assay artifact. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Later work defended a very rare mark while questioning whether that tiny amount explains biological effects. organism: Homo sapiens tissue_or_cell_type: Human histones H3/H4 in cultured cells experimental_model: Multiple antibody, radiotracer and cell-line comparisons of human histone biotinylation limitations: Authors estimated extremely low abundance and proposed HLCS chromatin scaffolding as a working model; nutritional epigenetic benefit was not demonstrated. exposure: Assay comparisons responding to artifact criticism evidence_span: {"source_cache": "artifacts/biotin-research/21930408.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "51af2341c7be0cb58c57e09784ebb8daabdd98cc93f04be52bb7b04b496e0b91", "start_char": 0, "end_char": 1318, "text_sha256": "51af2341c7be0cb58c57e09784ebb8daabdd98cc93f04be52bb7b04b496e0b91"} [b7-p21930408] Biotinylation is a natural, albeit rare, modification of human histones. (2011). https://pubmed.ncbi.nlm.nih.gov/21930408/ DOI: 10.1016/j.ymgme.2011.08.030
Complete structured claim and evidence
MS-SPI reported confirmed disability improvement in 13/103 biotin-treated patients versus 0/51 placebo patients at its primary endpoint (P=0.005).
Biotin → Confirmed disability improvement in progressive multiple sclerosis source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/27589059.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "78a9ac1eb5adeeb93272160336def9e0b07684dd1eb8a12978e7fa4782e69322", "start_char": 0, "end_char": 1333, "text_sha256": "78a9ac1eb5adeeb93272160336def9e0b07684dd1eb8a12978e7fa4782e69322"}
experimental_model
Randomized double-blind placebo-controlled MS-SPI trial in 154 adults
exposure
100 mg biotin three times daily for 12 months; later open treatment
limitations
Pharmacological exposure, not correction of proven nutritional deficiency. Small trial; larger confirmatory study did not reproduce efficacy.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
An early trial reported benefit in a subset of patients.
primary_references
[b7-p27589059] MD1003 (high-dose biotin) for the treatment of progressive multiple sclerosis: A randomised, double-blind, placebo-controlled study. (2016). https://pubmed.ncbi.nlm.nih.gov/27589059/ DOI: 10.1177/1352458516667568
tissue_or_cell_type
Progressive multiple sclerosis disability
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1196–1207
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled MS-SPI trial in 154 adults · source_derived_draft · unverified_draft
### b7-ms-early-benefit MS-SPI reported confirmed disability improvement in 13/103 biotin-treated patients versus 0/51 placebo patients at its primary endpoint (P=0.005). Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An early trial reported benefit in a subset of patients. organism: Homo sapiens tissue_or_cell_type: Progressive multiple sclerosis disability experimental_model: Randomized double-blind placebo-controlled MS-SPI trial in 154 adults limitations: Pharmacological exposure, not correction of proven nutritional deficiency. Small trial; larger confirmatory study did not reproduce efficacy. exposure: 100 mg biotin three times daily for 12 months; later open treatment evidence_span: {"source_cache": "artifacts/biotin-research/27589059.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "78a9ac1eb5adeeb93272160336def9e0b07684dd1eb8a12978e7fa4782e69322", "start_char": 0, "end_char": 1333, "text_sha256": "78a9ac1eb5adeeb93272160336def9e0b07684dd1eb8a12978e7fa4782e69322"} [b7-p27589059] MD1003 (high-dose biotin) for the treatment of progressive multiple sclerosis: A randomised, double-blind, placebo-controlled study. (2016). https://pubmed.ncbi.nlm.nih.gov/27589059/ DOI: 10.1177/1352458516667568
Complete structured claim and evidence
SPI2 found confirmed improvement in 39/326 biotin patients versus 29/316 placebo patients (odds ratio 1.35, 95% CI 0.81–2.26), without significant disability or walking-speed benefit.
Biotin → Confirmed disability improvement in progressive multiple sclerosis source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/33222767.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7665597ecbb900d0b66b45fcb92256f4d06a084811fbd914f0cdec82bd28aa00", "start_char": 0, "end_char": 3606, "text_sha256": "7665597ecbb900d0b66b45fcb92256f4d06a084811fbd914f0cdec82bd28aa00"}
experimental_model
SPI2 randomized double-blind placebo-controlled phase 3 trial; 642 randomized adults
exposure
100 mg biotin three times daily; primary improvement at month 12 confirmed at month 15
limitations
Pharmacologic dosing in a broader cohort; results do not address nutritional replacement in deficiency. Funding and assay-interference issues were reported.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
The larger confirmatory trial did not establish the hoped-for benefit.
primary_references
[b7-p33222767] Safety and efficacy of MD1003 (high-dose biotin) in patients with progressive multiple sclerosis (SPI2): a randomised, double-blind, placebo-controlled, phase 3 trial. (2020). https://pubmed.ncbi.nlm.nih.gov/33222767/ DOI: 10.1016/s1474-4422(20)30347-1
tissue_or_cell_type
Progressive multiple sclerosis disability
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1209–1220
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SPI2 randomized double-blind placebo-controlled phase 3 trial; 642 randomized adults · source_derived_draft · unverified_draft
### b7-ms-confirmatory-null SPI2 found confirmed improvement in 39/326 biotin patients versus 29/316 placebo patients (odds ratio 1.35, 95% CI 0.81–2.26), without significant disability or walking-speed benefit. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The larger confirmatory trial did not establish the hoped-for benefit. organism: Homo sapiens tissue_or_cell_type: Progressive multiple sclerosis disability experimental_model: SPI2 randomized double-blind placebo-controlled phase 3 trial; 642 randomized adults limitations: Pharmacologic dosing in a broader cohort; results do not address nutritional replacement in deficiency. Funding and assay-interference issues were reported. exposure: 100 mg biotin three times daily; primary improvement at month 12 confirmed at month 15 evidence_span: {"source_cache": "artifacts/biotin-research/33222767.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7665597ecbb900d0b66b45fcb92256f4d06a084811fbd914f0cdec82bd28aa00", "start_char": 0, "end_char": 3606, "text_sha256": "7665597ecbb900d0b66b45fcb92256f4d06a084811fbd914f0cdec82bd28aa00"} [b7-p33222767] Safety and efficacy of MD1003 (high-dose biotin) in patients with progressive multiple sclerosis (SPI2): a randomised, double-blind, placebo-controlled, phase 3 trial. (2020). https://pubmed.ncbi.nlm.nih.gov/33222767/ DOI: 10.1016/s1474-4422(20)30347-1
Complete structured claim and evidence
Excess specimen biotin can compete with biotinylated assay components for streptavidin capture.
Biotin → Streptavidin capture in biotinylated immunoassays source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/28973622.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ee7e5947d8391b7a0fa7601d8390147b99c5ff603b3462e9d1aa7f3db42b915", "start_char": 10835, "end_char": 11046, "text_sha256": "6961c53bc6d3c1e97eafba73060fb1498d9d349e555f112e7e3bceb48761dd0b"}
experimental_model
Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes
exposure
10 mg oral biotin daily for 7 days
limitations
Interference depends on assay architecture and version; this study does not establish current platform performance, a universal washout time or true hormone changes.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
The supplement can interfere with the measuring tool itself.
primary_references
[b7-p28973622] Association of Biotin Ingestion With Performance of Hormone and Nonhormone Assays in Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/28973622/ DOI: 10.1001/jama.2017.13705
tissue_or_cell_type
Blood specimens measured on named 2017 assay systems
trigger_kind
biomarker_context Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1222–1233
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes · source_derived_draft · unverified_draft
### b7-assay-capture Excess specimen biotin can compete with biotinylated assay components for streptavidin capture. Condition category: biomarker_context nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The supplement can interfere with the measuring tool itself. organism: Homo sapiens tissue_or_cell_type: Blood specimens measured on named 2017 assay systems experimental_model: Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes limitations: Interference depends on assay architecture and version; this study does not establish current platform performance, a universal washout time or true hormone changes. exposure: 10 mg oral biotin daily for 7 days evidence_span: {"source_cache": "artifacts/biotin-research/28973622.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ee7e5947d8391b7a0fa7601d8390147b99c5ff603b3462e9d1aa7f3db42b915", "start_char": 10835, "end_char": 11046, "text_sha256": "6961c53bc6d3c1e97eafba73060fb1498d9d349e555f112e7e3bceb48761dd0b"} [b7-p28973622] Association of Biotin Ingestion With Performance of Hormone and Nonhormone Assays in Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/28973622/ DOI: 10.1001/jama.2017.13705
Complete structured claim and evidence
Four of 15 biotinylated sandwich assays produced falsely lower results after the studied biotin regimen.
Biotin → Sandwich immunoassay reported result source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/28973622.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "522d4d4aa94ca55b26c48c5b04c23de73b9c9fc70d6e7bcf400ffa81c77b2beb", "start_char": 0, "end_char": 2478, "text_sha256": "522d4d4aa94ca55b26c48c5b04c23de73b9c9fc70d6e7bcf400ffa81c77b2beb"}
experimental_model
Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes
exposure
10 mg oral biotin daily for 7 days
limitations
Interference depends on assay architecture and version; this study does not establish current platform performance, a universal washout time or true hormone changes.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Some tests can read too low even though the substance in the body did not fall.
primary_references
[b7-p28973622] Association of Biotin Ingestion With Performance of Hormone and Nonhormone Assays in Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/28973622/ DOI: 10.1001/jama.2017.13705
tissue_or_cell_type
Blood specimens measured on named 2017 assay systems
trigger_kind
biomarker_context Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1235–1246
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes · source_derived_draft · unverified_draft
### b7-assay-sandwich Four of 15 biotinylated sandwich assays produced falsely lower results after the studied biotin regimen. Condition category: biomarker_context nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some tests can read too low even though the substance in the body did not fall. organism: Homo sapiens tissue_or_cell_type: Blood specimens measured on named 2017 assay systems experimental_model: Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes limitations: Interference depends on assay architecture and version; this study does not establish current platform performance, a universal washout time or true hormone changes. exposure: 10 mg oral biotin daily for 7 days evidence_span: {"source_cache": "artifacts/biotin-research/28973622.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "522d4d4aa94ca55b26c48c5b04c23de73b9c9fc70d6e7bcf400ffa81c77b2beb", "start_char": 0, "end_char": 2478, "text_sha256": "522d4d4aa94ca55b26c48c5b04c23de73b9c9fc70d6e7bcf400ffa81c77b2beb"} [b7-p28973622] Association of Biotin Ingestion With Performance of Hormone and Nonhormone Assays in Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/28973622/ DOI: 10.1001/jama.2017.13705
Complete structured claim and evidence
Five of eight biotinylated competitive assays produced falsely higher results after the studied biotin regimen.
Biotin → Competitive immunoassay reported result source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/28973622.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "522d4d4aa94ca55b26c48c5b04c23de73b9c9fc70d6e7bcf400ffa81c77b2beb", "start_char": 0, "end_char": 2478, "text_sha256": "522d4d4aa94ca55b26c48c5b04c23de73b9c9fc70d6e7bcf400ffa81c77b2beb"}
experimental_model
Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes
exposure
10 mg oral biotin daily for 7 days
limitations
Interference depends on assay architecture and version; this study does not establish current platform performance, a universal washout time or true hormone changes.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Other assay designs can produce the opposite error.
primary_references
[b7-p28973622] Association of Biotin Ingestion With Performance of Hormone and Nonhormone Assays in Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/28973622/ DOI: 10.1001/jama.2017.13705
tissue_or_cell_type
Blood specimens measured on named 2017 assay systems
trigger_kind
biomarker_context Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1248–1259
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes · source_derived_draft · unverified_draft
### b7-assay-competitive Five of eight biotinylated competitive assays produced falsely higher results after the studied biotin regimen. Condition category: biomarker_context nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Other assay designs can produce the opposite error. organism: Homo sapiens tissue_or_cell_type: Blood specimens measured on named 2017 assay systems experimental_model: Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes limitations: Interference depends on assay architecture and version; this study does not establish current platform performance, a universal washout time or true hormone changes. exposure: 10 mg oral biotin daily for 7 days evidence_span: {"source_cache": "artifacts/biotin-research/28973622.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "522d4d4aa94ca55b26c48c5b04c23de73b9c9fc70d6e7bcf400ffa81c77b2beb", "start_char": 0, "end_char": 2478, "text_sha256": "522d4d4aa94ca55b26c48c5b04c23de73b9c9fc70d6e7bcf400ffa81c77b2beb"} [b7-p28973622] Association of Biotin Ingestion With Performance of Hormone and Nonhormone Assays in Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/28973622/ DOI: 10.1001/jama.2017.13705
Complete structured claim and evidence
The studied Vitros 5600 PTH assay fell by a mean 61% after biotin, while serum calcium remained stable.
Biotin → Ortho Vitros 5600 PTH immunoassay result source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/28973622.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ee7e5947d8391b7a0fa7601d8390147b99c5ff603b3462e9d1aa7f3db42b915", "start_char": 20261, "end_char": 20798, "text_sha256": "440bd38aad94623f97cd7f956c63815b7a25d790328c4407bcdf6d24f8d2be0d"}
experimental_model
Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes
exposure
10 mg oral biotin daily for 7 days
limitations
Interference depends on assay architecture and version; this study does not establish current platform performance, a universal washout time or true hormone changes.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
A falsely low PTH result can misleadingly suggest a problem in calcium regulation.
primary_references
[b7-p28973622] Association of Biotin Ingestion With Performance of Hormone and Nonhormone Assays in Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/28973622/ DOI: 10.1001/jama.2017.13705
tissue_or_cell_type
Blood specimens measured on named 2017 assay systems
trigger_kind
biomarker_context Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1261–1272
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes · source_derived_draft · unverified_draft
### b7-assay-pth The studied Vitros 5600 PTH assay fell by a mean 61% after biotin, while serum calcium remained stable. Condition category: biomarker_context nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A falsely low PTH result can misleadingly suggest a problem in calcium regulation. organism: Homo sapiens tissue_or_cell_type: Blood specimens measured on named 2017 assay systems experimental_model: Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes limitations: Interference depends on assay architecture and version; this study does not establish current platform performance, a universal washout time or true hormone changes. exposure: 10 mg oral biotin daily for 7 days evidence_span: {"source_cache": "artifacts/biotin-research/28973622.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ee7e5947d8391b7a0fa7601d8390147b99c5ff603b3462e9d1aa7f3db42b915", "start_char": 20261, "end_char": 20798, "text_sha256": "440bd38aad94623f97cd7f956c63815b7a25d790328c4407bcdf6d24f8d2be0d"} [b7-p28973622] Association of Biotin Ingestion With Performance of Hormone and Nonhormone Assays in Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/28973622/ DOI: 10.1001/jama.2017.13705
Complete structured claim and evidence
The studied Vitros 5600 TSH assay showed a mean 94% decrease after biotin, with all results falling below its reference interval.
Biotin → Ortho Vitros 5600 TSH immunoassay result source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/28973622.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ee7e5947d8391b7a0fa7601d8390147b99c5ff603b3462e9d1aa7f3db42b915", "start_char": 19918, "end_char": 20260, "text_sha256": "2604315b772473fe3efb8d153000d7efcfac08a94ea918abe26153d29a429e3f"}
experimental_model
Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes
exposure
10 mg oral biotin daily for 7 days
limitations
Interference depends on assay architecture and version; this study does not establish current platform performance, a universal washout time or true hormone changes.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
This assay error can resemble suppressed thyroid-stimulating hormone.
primary_references
[b7-p28973622] Association of Biotin Ingestion With Performance of Hormone and Nonhormone Assays in Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/28973622/ DOI: 10.1001/jama.2017.13705
tissue_or_cell_type
Blood specimens measured on named 2017 assay systems
trigger_kind
biomarker_context Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1274–1285
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes · source_derived_draft · unverified_draft
### b7-assay-tsh The studied Vitros 5600 TSH assay showed a mean 94% decrease after biotin, with all results falling below its reference interval. Condition category: biomarker_context nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This assay error can resemble suppressed thyroid-stimulating hormone. organism: Homo sapiens tissue_or_cell_type: Blood specimens measured on named 2017 assay systems experimental_model: Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes limitations: Interference depends on assay architecture and version; this study does not establish current platform performance, a universal washout time or true hormone changes. exposure: 10 mg oral biotin daily for 7 days evidence_span: {"source_cache": "artifacts/biotin-research/28973622.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ee7e5947d8391b7a0fa7601d8390147b99c5ff603b3462e9d1aa7f3db42b915", "start_char": 19918, "end_char": 20260, "text_sha256": "2604315b772473fe3efb8d153000d7efcfac08a94ea918abe26153d29a429e3f"} [b7-p28973622] Association of Biotin Ingestion With Performance of Hormone and Nonhormone Assays in Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/28973622/ DOI: 10.1001/jama.2017.13705
Complete structured claim and evidence
The studied Roche cobas 25-hydroxyvitamin D assay increased falsely by a mean 9.25 ng/mL after biotin ingestion.
Biotin → Roche cobas e602 25-hydroxyvitamin D immunoassay result source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/biotin-research/28973622.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ee7e5947d8391b7a0fa7601d8390147b99c5ff603b3462e9d1aa7f3db42b915", "start_char": 30431, "end_char": 30652, "text_sha256": "65e440a45c3fe9c39d9a7a9cc537643507768c3dfac298d0a31d347e42c5ed28"}
experimental_model
Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes
exposure
10 mg oral biotin daily for 7 days
limitations
Interference depends on assay architecture and version; this study does not establish current platform performance, a universal washout time or true hormone changes.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
The apparent vitamin D rise was a measurement artifact.
primary_references
[b7-p28973622] Association of Biotin Ingestion With Performance of Hormone and Nonhormone Assays in Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/28973622/ DOI: 10.1001/jama.2017.13705
tissue_or_cell_type
Blood specimens measured on named 2017 assay systems
trigger_kind
biomarker_context Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1287–1298
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes · source_derived_draft · unverified_draft
### b7-assay-vitamin-d The studied Roche cobas 25-hydroxyvitamin D assay increased falsely by a mean 9.25 ng/mL after biotin ingestion. Condition category: biomarker_context nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The apparent vitamin D rise was a measurement artifact. organism: Homo sapiens tissue_or_cell_type: Blood specimens measured on named 2017 assay systems experimental_model: Nonrandomized crossover study of 6 healthy adults, 37 assays and 11 analytes limitations: Interference depends on assay architecture and version; this study does not establish current platform performance, a universal washout time or true hormone changes. exposure: 10 mg oral biotin daily for 7 days evidence_span: {"source_cache": "artifacts/biotin-research/28973622.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ee7e5947d8391b7a0fa7601d8390147b99c5ff603b3462e9d1aa7f3db42b915", "start_char": 30431, "end_char": 30652, "text_sha256": "65e440a45c3fe9c39d9a7a9cc537643507768c3dfac298d0a31d347e42c5ed28"} [b7-p28973622] Association of Biotin Ingestion With Performance of Hormone and Nonhormone Assays in Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/28973622/ DOI: 10.1001/jama.2017.13705
Complete structured claim and evidence
In the 10-man crossover study, biotin alone changed mean hair growth from 2.50 to 2.47 mm/week (P=0.53) over 14 days.
Biotin → Occipital hair growth rate in healthy men source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/38688776.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3f46962f37ad560b79a91a05d587ca0be1e5d52089a581d8920771d84b884d2c", "start_char": 4627, "end_char": 5539, "text_sha256": "3ead95bf33780d055dc9d137b66ac1359683d0c8e1adc16e58c14d598ea42625"}
experimental_model
Randomized-order open crossover study in 10 healthy men without hair disorders
exposure
14-day courses: oral biotin 5 mg/day, topical minoxidil 5%, or combination; 14-day washouts
limitations
Small, short, open study without placebo. Within-period significance in the combination does not establish a biochemical synergy or a treatment for alopecia.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Biotin alone did not speed hair growth in this small short experiment.
primary_references
[b7-p38688776] Efficacy of 5% topical minoxidil versus 5 mg oral biotin versus topical minoxidil and oral biotin on hair growth in men: randomized, crossover, clinical trial. (2024). https://pubmed.ncbi.nlm.nih.gov/38688776/ DOI: 10.1016/j.abd.2023.07.008
tissue_or_cell_type
Occipital hair growth
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1300–1311
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized-order open crossover study in 10 healthy men without hair disorders · source_derived_draft · unverified_draft
### b7-hair-biotin-alone In the 10-man crossover study, biotin alone changed mean hair growth from 2.50 to 2.47 mm/week (P=0.53) over 14 days. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Biotin alone did not speed hair growth in this small short experiment. organism: Homo sapiens tissue_or_cell_type: Occipital hair growth experimental_model: Randomized-order open crossover study in 10 healthy men without hair disorders limitations: Small, short, open study without placebo. Within-period significance in the combination does not establish a biochemical synergy or a treatment for alopecia. exposure: 14-day courses: oral biotin 5 mg/day, topical minoxidil 5%, or combination; 14-day washouts evidence_span: {"source_cache": "artifacts/biotin-research/38688776.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3f46962f37ad560b79a91a05d587ca0be1e5d52089a581d8920771d84b884d2c", "start_char": 4627, "end_char": 5539, "text_sha256": "3ead95bf33780d055dc9d137b66ac1359683d0c8e1adc16e58c14d598ea42625"} [b7-p38688776] Efficacy of 5% topical minoxidil versus 5 mg oral biotin versus topical minoxidil and oral biotin on hair growth in men: randomized, crossover, clinical trial. (2024). https://pubmed.ncbi.nlm.nih.gov/38688776/ DOI: 10.1016/j.abd.2023.07.008
Complete structured claim and evidence
The biotin-plus-topical-minoxidil period changed mean hair growth from 2.36 to 2.64 mm/week (P=0.02); the study did not establish a mechanistic nutrient-drug synergy.
Biotin → Occipital hair growth rate in healthy men source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/38688776.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3f46962f37ad560b79a91a05d587ca0be1e5d52089a581d8920771d84b884d2c", "start_char": 4627, "end_char": 5539, "text_sha256": "3ead95bf33780d055dc9d137b66ac1359683d0c8e1adc16e58c14d598ea42625"}
experimental_model
Randomized-order open crossover study in 10 healthy men without hair disorders
exposure
14-day courses: oral biotin 5 mg/day, topical minoxidil 5%, or combination; 14-day washouts
limitations
Small, short, open study without placebo. Within-period significance in the combination does not establish a biochemical synergy or a treatment for alopecia.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
A combination signal was observed, but its cause and long-term relevance remain uncertain.
primary_references
[b7-p38688776] Efficacy of 5% topical minoxidil versus 5 mg oral biotin versus topical minoxidil and oral biotin on hair growth in men: randomized, crossover, clinical trial. (2024). https://pubmed.ncbi.nlm.nih.gov/38688776/ DOI: 10.1016/j.abd.2023.07.008
tissue_or_cell_type
Occipital hair growth
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1313–1324
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized-order open crossover study in 10 healthy men without hair disorders · source_derived_draft · unverified_draft
### b7-hair-combination The biotin-plus-topical-minoxidil period changed mean hair growth from 2.36 to 2.64 mm/week (P=0.02); the study did not establish a mechanistic nutrient-drug synergy. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A combination signal was observed, but its cause and long-term relevance remain uncertain. organism: Homo sapiens tissue_or_cell_type: Occipital hair growth experimental_model: Randomized-order open crossover study in 10 healthy men without hair disorders limitations: Small, short, open study without placebo. Within-period significance in the combination does not establish a biochemical synergy or a treatment for alopecia. exposure: 14-day courses: oral biotin 5 mg/day, topical minoxidil 5%, or combination; 14-day washouts evidence_span: {"source_cache": "artifacts/biotin-research/38688776.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3f46962f37ad560b79a91a05d587ca0be1e5d52089a581d8920771d84b884d2c", "start_char": 4627, "end_char": 5539, "text_sha256": "3ead95bf33780d055dc9d137b66ac1359683d0c8e1adc16e58c14d598ea42625"} [b7-p38688776] Efficacy of 5% topical minoxidil versus 5 mg oral biotin versus topical minoxidil and oral biotin on hair growth in men: randomized, crossover, clinical trial. (2024). https://pubmed.ncbi.nlm.nih.gov/38688776/ DOI: 10.1016/j.abd.2023.07.008
Complete structured claim and evidence
After 28 days of experimental biotin depletion, leukocyte SLC19A3 RNA was 33% of baseline in seven adults.
Biotin → SLC19A3 RNA abundance source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Human biotin availability was associated with SLC19A3 expression; functional B1 deficiency was not established.
depleted-nutrient
Biotin · Biotin
evidence-scope
Blood leukocytes
evidence_locator
Abstract
evidence_spans
[{"source_document": "artifacts/thiamine_transport_sources/vlasova-2005-biotin-slc19a3-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1488}]
experimental_model
Seven evaluable adults before and after 28 days of an egg-white biotin-depleting diet.
limitations
No transporter protein, thiamine uptake or CNS endpoint measured.
nutrient_topic
Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
organism
Homo sapiens
plain_language
Low biotin changed expression of a B1-transporter gene.
primary_references
[vlasova-2005-biotin-slc19a3] Biotin deficiency reduces expression of SLC19A3, a potential biotin transporter, in leukocytes from human blood (2005). https://pubmed.ncbi.nlm.nih.gov/15623830/ DOI: 10.1093/jn/135.1.42
tissue_or_cell_type
Blood leukocytes
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 309–323
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Seven evaluable adults before and after 28 days of an egg-white biotin-depleting diet. · source_derived_draft · unverified_draft
### b1-biotin-depletion-slc19a3-rna After 28 days of experimental biotin depletion, leukocyte SLC19A3 RNA was 33% of baseline in seven adults. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low biotin changed expression of a B1-transporter gene. organism: Homo sapiens tissue_or_cell_type: Blood leukocytes experimental_model: Seven evaluable adults before and after 28 days of an egg-white biotin-depleting diet. limitations: No transporter protein, thiamine uptake or CNS endpoint measured. cross_nutrient: Human biotin availability was associated with SLC19A3 expression; functional B1 deficiency was not established. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/vlasova-2005-biotin-slc19a3-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1488}] evidence_locator: Abstract depleted-nutrient: Biotin evidence-scope: Blood leukocytes [vlasova-2005-biotin-slc19a3] Biotin deficiency reduces expression of SLC19A3, a potential biotin transporter, in leukocytes from human blood (2005). https://pubmed.ncbi.nlm.nih.gov/15623830/ DOI: 10.1093/jn/135.1.42
Complete structured claim and evidence
Family mapping identified recessive SLC19A3 variants in the disorder then called biotin-responsive basal ganglia disease.
SLC19A3 basal ganglia disease genotypes → SLC19A3 basal ganglia disease phenotype source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence-scope
Clinical genetics
evidence_locator
Abstract
evidence_spans
[{"source_document": "artifacts/thiamine_transport_sources/zeng-2005-slc19a3-genetics-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1170}]
experimental_model
Affected families; linkage mapping and sequence analysis.
limitations
Clinical response to biotin does not identify its molecular action.
nutrient_topic
Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
organism
Homo sapiens
plain_language
Inherited B1-transporter defects can cause severe neurological disease.
primary_references
[zeng-2005-slc19a3-genetics] Biotin-responsive basal ganglia disease maps to 2q36.3 and is due to mutations in SLC19A3 (2005). https://pubmed.ncbi.nlm.nih.gov/15871139/ DOI: 10.1086/431216
tissue_or_cell_type
Clinical genetics
trigger_kind
machinery_impairment Imported condition classification; unverified.
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 325–337
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Affected families; linkage mapping and sequence analysis. · source_derived_draft · unverified_draft
### b1-slc19a3-inherited-basal-ganglia Family mapping identified recessive SLC19A3 variants in the disorder then called biotin-responsive basal ganglia disease. Condition category: machinery_impairment nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Inherited B1-transporter defects can cause severe neurological disease. organism: Homo sapiens tissue_or_cell_type: Clinical genetics experimental_model: Affected families; linkage mapping and sequence analysis. limitations: Clinical response to biotin does not identify its molecular action. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/zeng-2005-slc19a3-genetics-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1170}] evidence_locator: Abstract evidence-scope: Clinical genetics [zeng-2005-slc19a3-genetics] Biotin-responsive basal ganglia disease maps to 2q36.3 and is due to mutations in SLC19A3 (2005). https://pubmed.ncbi.nlm.nih.gov/15871139/ DOI: 10.1086/431216
Complete structured claim and evidence
Wild-type SLC19A3 did not confer detectable biotin uptake, whereas the SLC5A6 positive control did.
Human thiamine transporter 2 / SLC19A3 → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Distinguishes thiamine transport from biotin transport; no shared-substrate mechanism demonstrated.
evidence-scope
Caco-2 and MDCK epithelial models
evidence_locator
Abstract
evidence_spans
[{"source_document": "artifacts/thiamine_transport_sources/subramanian-2006-biotin-specificity-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1656}]
experimental_model
Human transporter constructs in epithelial cell lines; uptake and surface targeting.
limitations
Tested cell models; clinical biotin-response mechanism remains unresolved.
nutrient_topic
Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
organism
Human proteins in human and canine cell lines
plain_language
The name biotin-responsive disease does not make SLC19A3 a biotin carrier.
primary_references
[subramanian-2006-biotin-specificity] Biotin-responsive basal ganglia disease-linked mutations inhibit thiamine transport via hTHTR2: biotin is not a substrate for hTHTR2 (2006). https://pubmed.ncbi.nlm.nih.gov/16790503/ DOI: 10.1152/ajpcell.00105.2006
tissue_or_cell_type
Caco-2 and MDCK epithelial models
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 294–307
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human transporter constructs in epithelial cell lines; uptake and surface targeting. · source_derived_draft · unverified_draft
### b1-slc19a3-not-biotin-transporter Wild-type SLC19A3 did not confer detectable biotin uptake, whereas the SLC5A6 positive control did. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The name biotin-responsive disease does not make SLC19A3 a biotin carrier. organism: Human proteins in human and canine cell lines tissue_or_cell_type: Caco-2 and MDCK epithelial models experimental_model: Human transporter constructs in epithelial cell lines; uptake and surface targeting. limitations: Tested cell models; clinical biotin-response mechanism remains unresolved. cross_nutrient: Distinguishes thiamine transport from biotin transport; no shared-substrate mechanism demonstrated. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/subramanian-2006-biotin-specificity-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1656}] evidence_locator: Abstract evidence-scope: Caco-2 and MDCK epithelial models [subramanian-2006-biotin-specificity] Biotin-responsive basal ganglia disease-linked mutations inhibit thiamine transport via hTHTR2: biotin is not a substrate for hTHTR2 (2006). https://pubmed.ncbi.nlm.nih.gov/16790503/ DOI: 10.1152/ajpcell.00105.2006
Complete structured claim and evidence
In seven adults, 28-day egg-white-induced biotin depletion reduced mean lymphocyte PCC activity to 23% of baseline.
Biotin → Human lymphocyte propionyl-CoA carboxylase activity source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
true
evidence_location
Primary abstract and indexed Results: PCC activity
experimental_model
Seven healthy adults
exposure
28-day egg-white-rich biotin-depletion diet
limitations
Lymphocyte enzyme activity; no concurrent B12 intervention or systemic pathway flux measurement.
nutrient_topic
Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
organism
Homo sapiens
plain_language
In this small depletion study, low biotin weakened a human enzyme upstream of B12-dependent metabolism.
primary_references
[stratton-2006-biotin] Lymphocyte propionyl-CoA carboxylase and its activation by biotin are sensitive indicators of marginal biotin deficiency in humans. (2006). https://pubmed.ncbi.nlm.nih.gov/16895887/ DOI: 10.1093/ajcn/84.1.384
tissue_or_cell_type
Peripheral blood lymphocytes
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1202–1214
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Seven healthy adults · source_derived_draft · unverified_draft
### biotin-depletion-lowers-pcc In seven adults, 28-day egg-white-induced biotin depletion reduced mean lymphocyte PCC activity to 23% of baseline. Condition category: nutrient_deficiency nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this small depletion study, low biotin weakened a human enzyme upstream of B12-dependent metabolism. organism: Homo sapiens tissue_or_cell_type: Peripheral blood lymphocytes experimental_model: Seven healthy adults limitations: Lymphocyte enzyme activity; no concurrent B12 intervention or systemic pathway flux measurement. exposure: 28-day egg-white-rich biotin-depletion diet cross_nutrient: true evidence_location: Primary abstract and indexed Results: PCC activity [stratton-2006-biotin] Lymphocyte propionyl-CoA carboxylase and its activation by biotin are sensitive indicators of marginal biotin deficiency in humans. (2006). https://pubmed.ncbi.nlm.nih.gov/16895887/ DOI: 10.1093/ajcn/84.1.384
Complete structured claim and evidence
PCC partially purified from control human fibroblasts contained biotin.
Human propionyl-CoA carboxylase / PCC → Biotin source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
evidence_location
Indexed primary abstract
experimental_model
Partially purified human fibroblast PCC
exposure
Control fibroblast enzyme fraction
limitations
Biotin content in an enzyme preparation; does not establish whole-body biotin thresholds.
nutrient_topic
Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
organism
Homo sapiens
plain_language
Human fibroblast PCC carried biotin, a different vitamin required upstream of the B12-dependent step.
primary_references
[hsia-1979-pcc] Human propionyl CoA carboxylase: some properties of the partially purified enzyme in fibroblasts from controls and patients with propionic acidemia. (1979). https://pubmed.ncbi.nlm.nih.gov/481943/ DOI: 10.1203/00006450-197906000-00005
tissue_or_cell_type
Fibroblasts
Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1145–1157
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Partially purified human fibroblast PCC · source_derived_draft · unverified_draft
### human-pcc-biotin PCC partially purified from control human fibroblasts contained biotin. Condition category: normal nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Human fibroblast PCC carried biotin, a different vitamin required upstream of the B12-dependent step. organism: Homo sapiens tissue_or_cell_type: Fibroblasts experimental_model: Partially purified human fibroblast PCC limitations: Biotin content in an enzyme preparation; does not establish whole-body biotin thresholds. exposure: Control fibroblast enzyme fraction cross_nutrient: true evidence_location: Indexed primary abstract [hsia-1979-pcc] Human propionyl CoA carboxylase: some properties of the partially purified enzyme in fibroblasts from controls and patients with propionic acidemia. (1979). https://pubmed.ncbi.nlm.nih.gov/481943/ DOI: 10.1203/00006450-197906000-00005
Complete structured claim and evidence
Mg depletion decreased liver crude-mitochondrial pyruvate-carboxylase activity; activity correlated positively with liver Mn concentration.
Magnesium → Rat hepatic pyruvate carboxylase activity source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Mg–Mn association with PC function; no demonstration of Mn-mediated rescue.
experimental_model
Forty 3-week-old male Wistar rats assigned Mg-deficient or control diets for two weeks
exposure
Mg-deficient versus normal synthetic diet for two weeks, starting at three weeks of age.
limitations
Correlation does not establish direct Mn causation. No human PC metal requirement or biotin-rescue claim is inferred.
nutrient_topic
Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
organism
Rattus norvegicus
plain_language
Lower PC activity accompanied the altered manganese status during rat magnesium depletion.
primary_references
[mn-enz-8773758] Tissue manganese levels and liver pyruvate carboxylase activity in magnesium-deficient rats. (1996). https://pubmed.ncbi.nlm.nih.gov/8773758/ DOI: 10.1007/bf02789459
tissue_or_cell_type
Liver crude mitochondrial fraction; tissues and plasma
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 685–696
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Forty 3-week-old male Wistar rats assigned Mg-deficient or control diets for two weeks · source_derived_draft · unverified_draft
### mn-enz-mg-depletion-pc Mg depletion decreased liver crude-mitochondrial pyruvate-carboxylase activity; activity correlated positively with liver Mn concentration. Condition category: nutrient_deficiency nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Lower PC activity accompanied the altered manganese status during rat magnesium depletion. organism: Rattus norvegicus tissue_or_cell_type: Liver crude mitochondrial fraction; tissues and plasma experimental_model: Forty 3-week-old male Wistar rats assigned Mg-deficient or control diets for two weeks limitations: Correlation does not establish direct Mn causation. No human PC metal requirement or biotin-rescue claim is inferred. exposure: Mg-deficient versus normal synthetic diet for two weeks, starting at three weeks of age. cross_nutrient: Mg–Mn association with PC function; no demonstration of Mn-mediated rescue. [mn-enz-8773758] Tissue manganese levels and liver pyruvate carboxylase activity in magnesium-deficient rats. (1996). https://pubmed.ncbi.nlm.nih.gov/8773758/ DOI: 10.1007/bf02789459
Complete structured claim and evidence
The inactive human ACC1 filament structure resolved acetyl-CoA in a pocket at the carboxyltransferase dimer interface.
Acetyl-CoA → Human acetyl-CoA carboxylase 1 / ACACA source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
evidence_location
Full text lines 101, 131; Fig. 4B
experimental_model
Endogenous human ACC1 purified from Expi293F cells and analyzed by cryo-EM
exposure
Substrate preparation contained 10 mM acetyl-CoA, 25 mM bicarbonate, 10 mM MgCl2 and 10 mM ATP; cryo-EM preparation conditions.
limitations
Ligand occupancy in an inactive structure is not an activity or dietary-repletion assay. Biotin density was not resolved in this map. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Acetyl-CoA binds the biotin-dependent carboxylase even in a structurally inactive state.
primary_references
[b5-met-acc2024] Filament structures unveil the dynamic organization of human acetyl-CoA carboxylase. (2024). https://pubmed.ncbi.nlm.nih.gov/39383219/ DOI: 10.1126/sciadv.ado4880
tissue_or_cell_type
Purified endogenous Expi293F ACC1
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1033–1045
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Endogenous human ACC1 purified from Expi293F cells and analyzed by cryo-EM · source_derived_draft · unverified_draft
### b5-met-acc-acetylcoa-binding The inactive human ACC1 filament structure resolved acetyl-CoA in a pocket at the carboxyltransferase dimer interface. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Acetyl-CoA binds the biotin-dependent carboxylase even in a structurally inactive state. organism: Homo sapiens tissue_or_cell_type: Purified endogenous Expi293F ACC1 experimental_model: Endogenous human ACC1 purified from Expi293F cells and analyzed by cryo-EM limitations: Ligand occupancy in an inactive structure is not an activity or dietary-repletion assay. Biotin density was not resolved in this map. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Substrate preparation contained 10 mM acetyl-CoA, 25 mM bicarbonate, 10 mM MgCl2 and 10 mM ATP; cryo-EM preparation conditions. cross_nutrient: true evidence_location: Full text lines 101, 131; Fig. 4B [b5-met-acc2024] Filament structures unveil the dynamic organization of human acetyl-CoA carboxylase. (2024). https://pubmed.ncbi.nlm.nih.gov/39383219/ DOI: 10.1126/sciadv.ado4880
Complete structured claim and evidence
Across 25, 250 and 10000 pmol/L biotin culture conditions for three weeks, biotin availability correlated negatively with SMVT protein abundance in human JAr cells.
Biotin → Human SLC5A6 protein abundance source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
true
experimental_model
Human JAr choriocarcinoma cells cultured for three weeks with deficient, physiological or pharmacological biotin
exposure
Three weeks at 25 pmol/L deficient, 250 pmol/L physiological, or 10000 pmol/L pharmacological biotin.
limitations
Tumor-derived placental cell model. The paper also measured biotin uptake and promoter activity, but a resulting change in pantothenate uptake or whole-placenta fetal delivery is not demonstrated by this abstract.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Cells exposed to less biotin made more of the transporter also used by B5.
primary_references
[b5-trans-biotin-supply2004] Biotin supply affects rates of cell proliferation, biotinylation of carboxylases and histones, and expression of the gene encoding the sodium-dependent multivitamin transporter in JAr choriocarcinoma cells. (2004). https://pubmed.ncbi.nlm.nih.gov/14991266/ DOI: 10.1007/s00394-004-0435-9
tissue_or_cell_type
JAr placental choriocarcinoma cells
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 327–338
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human JAr choriocarcinoma cells cultured for three weeks with deficient, physiological or pharmacological biotin · source_derived_draft · unverified_draft
### b5-trans-biotin-supply-smvt Across 25, 250 and 10000 pmol/L biotin culture conditions for three weeks, biotin availability correlated negatively with SMVT protein abundance in human JAr cells. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cells exposed to less biotin made more of the transporter also used by B5. organism: Homo sapiens tissue_or_cell_type: JAr placental choriocarcinoma cells experimental_model: Human JAr choriocarcinoma cells cultured for three weeks with deficient, physiological or pharmacological biotin limitations: Tumor-derived placental cell model. The paper also measured biotin uptake and promoter activity, but a resulting change in pantothenate uptake or whole-placenta fetal delivery is not demonstrated by this abstract. exposure: Three weeks at 25 pmol/L deficient, 250 pmol/L physiological, or 10000 pmol/L pharmacological biotin. cross_nutrient: true [b5-trans-biotin-supply2004] Biotin supply affects rates of cell proliferation, biotinylation of carboxylases and histones, and expression of the gene encoding the sodium-dependent multivitamin transporter in JAr choriocarcinoma cells. (2004). https://pubmed.ncbi.nlm.nih.gov/14991266/ DOI: 10.1007/s00394-004-0435-9
Complete structured claim and evidence
SLC5A6 knockdown analysis attributed 88.7% of total radiolabeled biotin uptake to SLC5A6 in human hCMEC/D3 brain endothelial cells.
Human sodium-dependent multivitamin transporter / SLC5A6 → Human brain endothelial biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
experimental_model
Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells
exposure
SLC5A6-specific siRNA and radiolabeled substrate uptake; tracer concentration not specified in the abstract.
limitations
Cellular luminal uptake is not itself a measurement of complete transendothelial delivery into brain tissue. Reported percentages apply to hCMEC/D3 under these assay conditions, not every human tissue.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
SMVT supplied most measured biotin uptake in the human brain endothelial cell model.
primary_references
[b5-trans-brain2015] Major involvement of Na(+) -dependent multivitamin transporter (SLC5A6/SMVT) in uptake of biotin and pantothenic acid by human brain capillary endothelial cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25809983/ DOI: 10.1111/jnc.13092
tissue_or_cell_type
hCMEC/D3 cerebral microvascular endothelial cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 288–299
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells · source_derived_draft · unverified_draft
### b5-trans-brain-biotin SLC5A6 knockdown analysis attributed 88.7% of total radiolabeled biotin uptake to SLC5A6 in human hCMEC/D3 brain endothelial cells. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT supplied most measured biotin uptake in the human brain endothelial cell model. organism: Homo sapiens tissue_or_cell_type: hCMEC/D3 cerebral microvascular endothelial cells experimental_model: Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells limitations: Cellular luminal uptake is not itself a measurement of complete transendothelial delivery into brain tissue. Reported percentages apply to hCMEC/D3 under these assay conditions, not every human tissue. exposure: SLC5A6-specific siRNA and radiolabeled substrate uptake; tracer concentration not specified in the abstract. cross_nutrient: true [b5-trans-brain2015] Major involvement of Na(+) -dependent multivitamin transporter (SLC5A6/SMVT) in uptake of biotin and pantothenic acid by human brain capillary endothelial cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25809983/ DOI: 10.1111/jnc.13092
Complete structured claim and evidence
Intestine-specific Slc5a6 deletion completely inhibited the measured carrier-mediated intestinal biotin uptake component relative to littermate controls.
Intestine-specific Slc5a6-null mouse genotype → Mouse intestinal carrier-mediated biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
experimental_model
Intestine-specific Slc5a6 conditional knockout mice compared with sex-matched littermates; in vivo and in vitro uptake
exposure
Cre/lox-mediated intestinal Slc5a6 deletion; in vivo and in vitro biotin transport assays.
limitations
This is shared transporter machinery impairment, not a dietary B5 depletion experiment. The abstract directly reports biotin uptake; no numerical pantothenate or lipoate absorption deficit is inferred. Passive uptake outside the measured carrier component is not excluded.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Mus musculus
plain_language
Removing the shared vitamin transporter eliminated active intestinal biotin uptake in these mice.
primary_references
[b5-trans-intestinal-knockout2013] Conditional knockout of the Slc5a6 gene in mouse intestine impairs biotin absorption. (2013). https://pubmed.ncbi.nlm.nih.gov/23104561/ DOI: 10.1152/ajpgi.00379.2012
tissue_or_cell_type
Intestinal epithelium
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 314–325
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestine-specific Slc5a6 conditional knockout mice compared with sex-matched littermates; in vivo and in vitro uptake · source_derived_draft · unverified_draft
### b5-trans-intestinal-knockout-biotin Intestine-specific Slc5a6 deletion completely inhibited the measured carrier-mediated intestinal biotin uptake component relative to littermate controls. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing the shared vitamin transporter eliminated active intestinal biotin uptake in these mice. organism: Mus musculus tissue_or_cell_type: Intestinal epithelium experimental_model: Intestine-specific Slc5a6 conditional knockout mice compared with sex-matched littermates; in vivo and in vitro uptake limitations: This is shared transporter machinery impairment, not a dietary B5 depletion experiment. The abstract directly reports biotin uptake; no numerical pantothenate or lipoate absorption deficit is inferred. Passive uptake outside the measured carrier component is not excluded. exposure: Cre/lox-mediated intestinal Slc5a6 deletion; in vivo and in vitro biotin transport assays. cross_nutrient: true [b5-trans-intestinal-knockout2013] Conditional knockout of the Slc5a6 gene in mouse intestine impairs biotin absorption. (2013). https://pubmed.ncbi.nlm.nih.gov/23104561/ DOI: 10.1152/ajpgi.00379.2012
Complete structured claim and evidence
Oxidized alpha-lipoic acid inhibited human SMVT-mediated radiolabeled biotin uptake with an IC50 of 9.1 micromolar in the 2026 HEK293T assay.
Lipoic acid → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells
exposure
Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied.
limitations
In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Oxidized alpha-lipoic acid competed with biotin uptake in the SMVT cell assay.
primary_references
[b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
tissue_or_cell_type
HEK293T cells expressing human SMVT
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 444–455
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells · source_derived_draft · unverified_draft
### b5-trans-lipoate-inhibits-biotin Oxidized alpha-lipoic acid inhibited human SMVT-mediated radiolabeled biotin uptake with an IC50 of 9.1 micromolar in the 2026 HEK293T assay. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Oxidized alpha-lipoic acid competed with biotin uptake in the SMVT cell assay. organism: Homo sapiens tissue_or_cell_type: HEK293T cells expressing human SMVT experimental_model: Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells limitations: In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency. exposure: Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied. cross_nutrient: true [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
Complete structured claim and evidence
D-pantothenic acid inhibited human SMVT-mediated radiolabeled biotin uptake with an IC50 of 89.7 micromolar in the 2026 HEK293T assay.
Pantothenate (vitamin B5) → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells
exposure
Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied.
limitations
In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
D-pantothenic acid competed with biotin uptake in the SMVT cell assay.
primary_references
[b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
tissue_or_cell_type
HEK293T cells expressing human SMVT
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 431–442
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells · source_derived_draft · unverified_draft
### b5-trans-pantothenate-inhibits-biotin D-pantothenic acid inhibited human SMVT-mediated radiolabeled biotin uptake with an IC50 of 89.7 micromolar in the 2026 HEK293T assay. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: D-pantothenic acid competed with biotin uptake in the SMVT cell assay. organism: Homo sapiens tissue_or_cell_type: HEK293T cells expressing human SMVT experimental_model: Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells limitations: In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency. exposure: Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied. cross_nutrient: true [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
Complete structured claim and evidence
Fibroblasts from the proband with SLC5A6 c.393+2T>C and p.Ser429Gly variants showed approximately 90% lower biotin uptake than controls.
Human SLC5A6 c.393+2T>C / p.Ser429Gly genotype → Human fibroblast biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
experimental_model
Patient-derived fibroblasts in a human SLC5A6 family study; molecular and radiolabeled biotin uptake analysis
exposure
The p.Ser429Gly allele supplied canonically spliced transcripts in the compound-heterozygous proband; uptake compared with control fibroblasts.
limitations
Abstract-only transport extraction. This is one proband genotype, not an isolated p.Ser429Gly dose-response study; neither pantothenate uptake nor the relative contribution of individual supplements is quantified.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
A patient with two SLC5A6 variants had a large defect in cellular biotin entry.
primary_references
[b5-trans-neuropathy2024] Genome sequencing enables diagnosis and treatment of SLC5A6 neuropathy. (2024). https://pubmed.ncbi.nlm.nih.gov/38816490/ DOI: 10.1038/s41431-024-01641-8
tissue_or_cell_type
Patient-derived fibroblasts
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 392–403
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient-derived fibroblasts in a human SLC5A6 family study; molecular and radiolabeled biotin uptake analysis · source_derived_draft · unverified_draft
### b5-trans-patient-fibroblast-biotin Fibroblasts from the proband with SLC5A6 c.393+2T>C and p.Ser429Gly variants showed approximately 90% lower biotin uptake than controls. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A patient with two SLC5A6 variants had a large defect in cellular biotin entry. organism: Homo sapiens tissue_or_cell_type: Patient-derived fibroblasts experimental_model: Patient-derived fibroblasts in a human SLC5A6 family study; molecular and radiolabeled biotin uptake analysis limitations: Abstract-only transport extraction. This is one proband genotype, not an isolated p.Ser429Gly dose-response study; neither pantothenate uptake nor the relative contribution of individual supplements is quantified. exposure: The p.Ser429Gly allele supplied canonically spliced transcripts in the compound-heterozygous proband; uptake compared with control fibroblasts. cross_nutrient: true [b5-trans-neuropathy2024] Genome sequencing enables diagnosis and treatment of SLC5A6 neuropathy. (2024). https://pubmed.ncbi.nlm.nih.gov/38816490/ DOI: 10.1038/s41431-024-01641-8
Complete structured claim and evidence
Extracellular pantothenate did not significantly change biotin efflux from radiolabeled-biotin-loaded human peripheral blood mononuclear cells.
Pantothenate (vitamin B5) → Human peripheral blood mononuclear cell biotin efflux source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays
exposure
[3H]biotin-loaded PBMC challenged with extracellular pantothenate; efflux-specific concentration not supplied in the abstract.
limitations
P greater than 0.05 is a null result in this assay, not proof of no effect under every condition. The experiment does not identify a general B5 export transporter or SMVT-mediated exchange mechanism.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Adding B5 outside these blood cells did not drive biotin back out.
primary_references
[b5-trans-pbmc1999] Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor. (1999). https://pubmed.ncbi.nlm.nih.gov/15539319/ DOI: 10.1016/s0955-2863(99)00024-8
tissue_or_cell_type
Isolated peripheral blood mononuclear cells
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 470–481
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays · source_derived_draft · unverified_draft
### b5-trans-pbmc-efflux-null Extracellular pantothenate did not significantly change biotin efflux from radiolabeled-biotin-loaded human peripheral blood mononuclear cells. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding B5 outside these blood cells did not drive biotin back out. organism: Homo sapiens tissue_or_cell_type: Isolated peripheral blood mononuclear cells experimental_model: Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays limitations: P greater than 0.05 is a null result in this assay, not proof of no effect under every condition. The experiment does not identify a general B5 export transporter or SMVT-mediated exchange mechanism. exposure: [3H]biotin-loaded PBMC challenged with extracellular pantothenate; efflux-specific concentration not supplied in the abstract. cross_nutrient: true [b5-trans-pbmc1999] Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor. (1999). https://pubmed.ncbi.nlm.nih.gov/15539319/ DOI: 10.1016/s0955-2863(99)00024-8
Complete structured claim and evidence
Pantothenate at 10–1000 nmol/L reduced uptake of 475 pmol/L biotin by less than 12% in isolated human peripheral blood mononuclear cells.
Pantothenate (vitamin B5) → Human peripheral blood mononuclear cell biotin uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays
exposure
10–1000 nmol/L pantothenic acid with 475 pmol/L [3H]biotin.
limitations
Cell-type-specific assay; the transporter was not molecularly identified as SLC5A6. This does not negate shared SMVT competition in other models and does not test high-dose supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
At the tested physiological concentrations, B5 only slightly reduced biotin entry into these blood cells.
primary_references
[b5-trans-pbmc1999] Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor. (1999). https://pubmed.ncbi.nlm.nih.gov/15539319/ DOI: 10.1016/s0955-2863(99)00024-8
tissue_or_cell_type
Isolated peripheral blood mononuclear cells
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 457–468
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays · source_derived_draft · unverified_draft
### b5-trans-pbmc-small-competition Pantothenate at 10–1000 nmol/L reduced uptake of 475 pmol/L biotin by less than 12% in isolated human peripheral blood mononuclear cells. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: At the tested physiological concentrations, B5 only slightly reduced biotin entry into these blood cells. organism: Homo sapiens tissue_or_cell_type: Isolated peripheral blood mononuclear cells experimental_model: Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays limitations: Cell-type-specific assay; the transporter was not molecularly identified as SLC5A6. This does not negate shared SMVT competition in other models and does not test high-dose supplementation. exposure: 10–1000 nmol/L pantothenic acid with 475 pmol/L [3H]biotin. cross_nutrient: true [b5-trans-pbmc1999] Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor. (1999). https://pubmed.ncbi.nlm.nih.gov/15539319/ DOI: 10.1016/s0955-2863(99)00024-8
Complete structured claim and evidence
Expression of human SLC5A6 R123L failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake.
Human SLC5A6 R123L protein variant → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
experimental_model
Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants
exposure
Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake.
limitations
Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The R123L SMVT variant lost the uptake activity seen with the normal transporter.
primary_references
[b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
tissue_or_cell_type
HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 353–364
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants · source_derived_draft · unverified_draft
### b5-trans-r123l-biotin Expression of human SLC5A6 R123L failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The R123L SMVT variant lost the uptake activity seen with the normal transporter. organism: Homo sapiens tissue_or_cell_type: HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells experimental_model: Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants limitations: Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency. exposure: Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake. cross_nutrient: true [b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
Complete structured claim and evidence
Expression of human SLC5A6 R94X failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake.
Human SLC5A6 R94X truncated protein → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
experimental_model
Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants
exposure
Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake.
limitations
Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The R94X SMVT variant lost the uptake activity seen with the normal transporter.
primary_references
[b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
tissue_or_cell_type
HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 340–351
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants · source_derived_draft · unverified_draft
### b5-trans-r94x-biotin Expression of human SLC5A6 R94X failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The R94X SMVT variant lost the uptake activity seen with the normal transporter. organism: Homo sapiens tissue_or_cell_type: HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells experimental_model: Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants limitations: Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency. exposure: Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake. cross_nutrient: true [b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
Complete structured claim and evidence
Human SMVT cryo-EM complexes placed pantothenate, biotin and oxidized lipoate in substantially overlapping positions within one central substrate-binding pocket.
Human sodium-dependent multivitamin transporter / SLC5A6 → Pantothenate (vitamin B5) source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells
exposure
SMVTEM/NbALFA complexes incubated with 2 mM D-pantothenic acid, 4 mM biotin or 22 mM oxidized alpha-lipoic acid for separate structures.
limitations
Engineered, purified transporter structure supports a binding mechanism; it does not establish nutritional competition severity in vivo. The structural construct has altered biotin transport kinetics relative to wild type. These are separate ligand-bound complexes, not simultaneous occupancy.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
B5, biotin and free lipoate use the same binding pocket in SMVT.
primary_references
[b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
tissue_or_cell_type
Purified human SMVT; HEK293-derived expression system
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 405–416
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells · source_derived_draft · unverified_draft
### b5-trans-shared-substrate-site Human SMVT cryo-EM complexes placed pantothenate, biotin and oxidized lipoate in substantially overlapping positions within one central substrate-binding pocket. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: B5, biotin and free lipoate use the same binding pocket in SMVT. organism: Homo sapiens tissue_or_cell_type: Purified human SMVT; HEK293-derived expression system experimental_model: Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells limitations: Engineered, purified transporter structure supports a binding mechanism; it does not establish nutritional competition severity in vivo. The structural construct has altered biotin transport kinetics relative to wild type. These are separate ligand-bound complexes, not simultaneous occupancy. exposure: SMVTEM/NbALFA complexes incubated with 2 mM D-pantothenic acid, 4 mM biotin or 22 mM oxidized alpha-lipoic acid for separate structures. cross_nutrient: true [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
Complete structured claim and evidence
Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of biotin.
Human sodium-dependent multivitamin transporter / SLC5A6 → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes
exposure
Human SMVT cDNA expression; substrate concentrations not specified in the abstract.
limitations
Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens (protein and HRPE expression cells)
plain_language
SMVT carries biotin into cells using sodium-dependent transport.
primary_references
[b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
tissue_or_cell_type
HRPE cell plasma membrane
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 171–182
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes · source_derived_draft · unverified_draft
### b5-trans-smvt-biotin Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of biotin. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT carries biotin into cells using sodium-dependent transport. organism: Homo sapiens (protein and HRPE expression cells) tissue_or_cell_type: HRPE cell plasma membrane experimental_model: Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes limitations: Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. exposure: Human SMVT cDNA expression; substrate concentrations not specified in the abstract. cross_nutrient: true [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

Alcohol exposure can reduce biotin entry

Condition: machinery_impairment · Chronic ethanol exposure in the specified model.

Normal role: Intestinal transport brings absorbed biotin into the body.

Recorded consequence: Transporter expression and measured uptake fall.

Scope: Human intestinal cells and separate rodent experiments

Biotin conservation can fail at the kidney

Condition: machinery_impairment · Chronic ethanol exposure in HK-2 cells.

Normal role: Renal uptake contributes to reclaiming filtered biotin.

Recorded consequence: Biotin uptake and SLC5A6 promoter activity decline.

Scope: Human renal cell culture

SMVT supplied most measured biotin uptake in the human brain endothelial cell model.

Condition: machinery_impairment · Experimental SLC5A6-specific siRNA knockdown in human brain endothelial cells, used to estimate the transporter contribution to uptake.

Normal role: SMVT supports cellular availability of pantothenate, biotin and lipoate through shared transport machinery.

Recorded consequence: SLC5A6 knockdown analysis attributed 88.7% of total radiolabeled biotin uptake to SLC5A6 in human hCMEC/D3 brain endothelial cells.

Scope: Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells; SLC5A6-specific siRNA and radiolabeled substrate uptake; tracer concentration not specified in the abstract.

Some drugs compete with intestinal biotin uptake

Condition: machinery_impairment · Carbamazepine or primidone in isolated membrane assays.

Normal role: Brush-border transport admits biotin from the gut.

Recorded consequence: Competitive inhibition at the brush border; basolateral transport was unaffected.

Scope: Human intestinal membrane preparations

Removing the shared vitamin transporter eliminated active intestinal biotin uptake in these mice.

Condition: machinery_impairment · Intestine-specific genetic deletion of mouse Slc5a6.

Normal role: SMVT supports cellular availability of pantothenate, biotin and lipoate through shared transport machinery.

Recorded consequence: Intestine-specific Slc5a6 deletion completely inhibited the measured carrier-mediated intestinal biotin uptake component relative to littermate controls.

Scope: Intestine-specific Slc5a6 conditional knockout mice compared with sex-matched littermates; in vivo and in vitro uptake; Cre/lox-mediated intestinal Slc5a6 deletion; in vivo and in vitro biotin transport assays.

Biotin turnover markers may change during drug treatment

Condition: biomarker_context · Long-term anticonvulsant treatment in a small pediatric comparison.

Normal role: Biotin turnover and enzyme function contribute different biomarker signals.

Recorded consequence: Some catabolites and 3-HIA rise while urinary biotin is usually not low.

Scope: Children receiving anticonvulsants

Cells exposed to less biotin made more of the transporter also used by B5.

Condition: nutrient_deficiency · Experimentally reduced extracellular biotin availability (25 versus 250 pmol/L), within a three-level biotin-supply experiment.

Normal role: SMVT supports cellular availability of pantothenate, biotin and lipoate through shared transport machinery.

Recorded consequence: Across 25, 250 and 10000 pmol/L biotin culture conditions for three weeks, biotin availability correlated negatively with SMVT protein abundance in human JAr cells.

Scope: Human JAr choriocarcinoma cells cultured for three weeks with deficient, physiological or pharmacological biotin; Three weeks at 25 pmol/L deficient, 250 pmol/L physiological, or 10000 pmol/L pharmacological biotin.

The biotin recycling step can fail

Condition: machinery_impairment · Inherited very low biotinidase activity.

Normal role: Biotinidase releases reusable biotin from biotinylated breakdown products.

Recorded consequence: Recycling fails and several biotin-dependent enzymes can become under-supplied.

Scope: Human biotinidase deficiency

The R94X SMVT variant lost the uptake activity seen with the normal transporter.

Condition: machinery_impairment · Expression of patient-associated SLC5A6 R94X protein variant.

Normal role: SMVT supports cellular availability of pantothenate, biotin and lipoate through shared transport machinery.

Recorded consequence: Expression of human SLC5A6 R94X failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake.

Scope: Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants; Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake.

Having biotin is not enough when its attachment enzyme is impaired

Condition: machinery_impairment · An inherited HLCS variant reduces catalytic activity or biotin affinity.

Normal role: HLCS activates biotin and attaches it to carboxylases.

Recorded consequence: Several pathways may fail; the biochemical response to extra biotin depends on residual enzyme function.

Scope: Human HLCS deficiency

The R123L SMVT variant lost the uptake activity seen with the normal transporter.

Condition: machinery_impairment · Expression of patient-associated SLC5A6 R123L protein variant.

Normal role: SMVT supports cellular availability of pantothenate, biotin and lipoate through shared transport machinery.

Recorded consequence: Expression of human SLC5A6 R123L failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake.

Early treatment can bypass a recycling shortage

Condition: machinery_impairment · Screen-detected biotinidase deficiency treated from birth.

Normal role: Recycling normally conserves biotin.

Recorded consequence: Most adherent children developed normally in the reported cohort.

Scope: Newborn-screened human biotinidase deficiency

Less ACC2 can release a brake on fat oxidation

Condition: machinery_impairment · Genetic Acacb deletion in mice.

Normal role: ACC2 contributes to a local malonyl-CoA pool involved in regulating fat oxidation.

Recorded consequence: Muscle malonyl-CoA decreased and fat oxidation increased.

Scope: Acacb-knockout mice

Loss of PC reaches beyond glucose production

Condition: machinery_impairment · Liver-specific Pcx deletion in mice.

Normal role: PC supplies oxaloacetate to support TCA-cycle intermediates and downstream metabolism.

Recorded consequence: Glucose production, nitrogen handling and antioxidant pools were disrupted.

Scope: Mouse liver-specific knockout

A patient with two SLC5A6 variants had a large defect in cellular biotin entry.

Condition: machinery_impairment · Biallelic SLC5A6 variants affecting canonical transcript production and transporter function.

Normal role: SMVT supports cellular availability of pantothenate, biotin and lipoate through shared transport machinery.

Recorded consequence: Fibroblasts from the proband with SLC5A6 c.393+2T>C and p.Ser429Gly variants showed approximately 90% lower biotin uptake than controls.

Scope: Patient-derived fibroblasts in a human SLC5A6 family study; molecular and radiolabeled biotin uptake analysis; The p.Ser429Gly allele supplied canonically spliced transcripts in the compound-heterozygous proband; uptake compared with control fibroblasts.

Impaired PC can reduce antioxidant support in islets

Condition: machinery_impairment · PC knockdown in human islets under nitrosative stress.

Normal role: PC-linked carbon metabolism helps sustain glutathione.

Recorded consequence: The glutathione pool and reduced-to-oxidized ratio fall.

Scope: Primary human pancreatic-islet experiments

Low available biotin changes leucine breakdown

Condition: nutrient_deficiency · Experimental egg-white-induced biotin depletion.

Normal role: Biotin-loaded MCC processes methylcrotonyl-CoA during leucine metabolism.

Recorded consequence: Urinary 3-HIA rises and improves during repletion.

Scope: Healthy adult experimental depletion

Low carnitine can hide a biotin-deficiency signal

Condition: nutrient_deficiency · Biotin deficiency with or without carnitine deficiency.

Normal role: Carnitine permits formation of acylcarnitines that can reveal an upstream metabolic bottleneck.

Recorded consequence: C5-OH can stay low during dual depletion and rise sharply when carnitine is restored.

Scope: Human HepG2 cell model

Pregnancy changes how biotin markers should be read

Condition: biomarker_context · Pregnancy or lactation under controlled intake.

Normal role: Biotin-dependent leucine metabolism contributes to urinary markers.

Recorded consequence: Markers change in different directions rather than providing one universal biotin reading.

Scope: Pregnant, lactating and control women

Fetal responses to biotin shortage differ by species

Condition: nutrient_deficiency · Maternal deprivation in rodent experiments.

Normal role: Maternal supply contributes to fetal biotin availability.

Recorded consequence: Mouse malformations, no observed rat malformations, and high hamster embryonic loss differed by species.

Scope: Rodent gestation

A specific enzyme defect can resemble a biotin-related blockage

Condition: machinery_impairment · Inherited MCCC1 or MCCC2 defect.

Normal role: MCC processes an intermediate of leucine breakdown.

Recorded consequence: Biochemical abnormalities can occur with variable clinical consequences.

Scope: Human isolated MCC deficiency

More than one missing vitamin can disrupt the metabolic picture

Condition: nutrient_deficiency · Combined vitamin deficiency during prolonged parenteral nutrition in premature twins.

Normal role: B2- and B7-dependent enzymes support distinct metabolic reactions.

Recorded consequence: Severe metabolic abnormalities occurred; the surviving twin improved after combined replacement.

Scope: Premature neonatal case report

Biotin shortage can alter immune-cell signaling

Condition: nutrient_deficiency · Biotin-deficient culture during T-cell stimulation.

Normal role: Adequate cofactors support cellular metabolic regulation.

Recorded consequence: Proinflammatory signals rose and regulatory-cell measures fell.

Scope: Human activated CD4 T-cell culture

A transporter can be present but poorly positioned

Condition: machinery_impairment · LPS exposure in colonic-cell experiments.

Normal role: SMVT must reach the cell surface to transport biotin.

Recorded consequence: Less surface transporter and less uptake occurred despite unchanged total protein and RNA.

Scope: Human colonic-cell model

Diet and microbes can jointly reduce available biotin

Condition: nutrient_deficiency · Biotin-deprived diet with antibiotic-induced dysbiosis or experimental L. murinus colonization.

Normal role: Dietary supply and microbial use affect luminal biotin.

Recorded consequence: Luminal biotin fell and alopecia appeared in the specified mouse models.

Scope: Mouse diet-microbiota experiments

Biotin can change a laboratory result without changing the hormone

Condition: biomarker_context · Excess specimen biotin after supplementation.

Normal role: Biotin-streptavidin capture is part of some laboratory assay designs.

Recorded consequence: Certain sandwich tests read falsely low and competitive tests falsely high.

Scope: Specific biotinylated blood-test systems

In this small depletion study, low biotin weakened a human enzyme upstream of B12-dependent metabolism.

Condition: nutrient_deficiency · 28-day egg-white-rich biotin-depletion diet

Normal role: Adenosylcobalamin-dependent propionyl-CoA metabolism requires intact upstream enzymes, MMAB, MMAA and MMUT.

Recorded consequence: In seven adults, 28-day egg-white-induced biotin depletion reduced mean lymphocyte PCC activity to 23% of baseline.

Scope: Peripheral blood lymphocytes; Homo sapiens

The sources

Every document behind this chapter is preserved word for word. Open one to read it in full with its recorded conflicts marked in place.

Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source

Recorded disagreements

Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.

High-dose biotin in progressive MS: early benefit did not replicateThe trials reached different efficacy conclusions. MS-SPI was smaller, had no placebo responders and used different eligibility and confirmation timing from the broader SPI2 trial. Those differences and random variation are candidate explanations, not proven mechanisms of the discrepant result.Read the recorded disagreement
Histone biotinylation: assay artifact, rare modification, or functional regulator?The published studies explicitly dispute the interpretation and specificity of histone-biotin measurements. This is not a conflict between the numerical bounds: less than 0.001% is compatible with less than 0.03%. Peptide assays, antibody specificity, streptavidin binding and radiotracer sensitivity address different parts of the dispute.Read the recorded disagreement

Open questions in this collection

Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.

Does HLCS substrate preference determine a reproducible human tissue hierarchy during dietary biotin restriction?Purified acceptor-fragment kinetics do not specify tissue transport, enzyme turnover or a universal order of failure.
How is biotin delivered into each subcellular compartment and how is mitochondrial cofactor attachment coordinated with protein import?The selected experiments support attachment-site recognition but do not identify every transport and allocation step.
Does biotin restriction reproduce the redox changes seen after liver PC deletion in humans?The knockout establishes a role of the enzyme; it does not measure a biotin threshold or show that extra biotin raises glutathione in a replete person.
How should combined B7, B12, B5 and mineral deficits be weighted along propionyl-CoA processing?Individual steps are linked, but the ledger does not yet contain a controlled human experiment testing the complete combined-deficiency chain.
Which mechanisms explain changes in biotin status during pregnancy and lactation, and which markers best track functional sufficiency?Controlled feeding showed discordant markers, while the carnitine-masking mechanism was tested in HepG2 cells rather than prospectively validated in pregnant people.
Can any common hair or nail complaint in a biotin-replete person be reliably improved by biotin alone?Deficiency rescue, combined interventions and small short trials do not establish broad cosmetic efficacy.
What causes the differing responses between the two progressive-MS trials?Trial size, placebo response, population and endpoint timing differ; a biological responder subgroup has not been established by the cited studies.
Is histone biotinylation causally important at the reported low abundance?Assay specificity and proposed HLCS chromatin-scaffolding functions remain separate from proof that a rare covalent mark regulates transcription.
What specimen handling is sufficient for each present-day biotin-sensitive assay?Platform versions, assay architecture, dose, time since ingestion and clearance matter; the 2017 study is not a universal current washout rule.
How much does bacterial biotin production contribute to usable human biotin across diets and microbiomes?Colonic uptake and animal microbiome experiments do not quantify whole-body human supply.
When does B5 or lipoate competition meaningfully reduce biotin status in people?Shared transport and in-vitro inhibition do not establish a dietary dose at which clinically important deficiency occurs.

Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.

Evidence, AI assistance and curation standards

Biotin

The mechanisms

HLCS activates biotin with ATP to form enzyme-bound biotinyl-5-prime-AMP before transferring biotin to a carboxylase acceptor.

HLCS transfers the activated biotin moiety to the epsilon-amino group of a specific lysine in a carboxylase biotin-acceptor domain.

Biotinidase releases biotin from its linkage to the epsilon-amino group of lysine, allowing the cofactor to be reused.

Human PC catalyzes two-step pyruvate carboxylation to oxaloacetate.

Human PCC supplies (S)-methylmalonyl-CoA by propionyl-CoA carboxylation upstream of the MCEE-MMUT sequence examined in fibroblast assays.

Human MCEE interconverts methylmalonyl-CoA epimers, supplying the (R) form for MMUT; MCEE expression increased coupled succinate production.

Adenosylcobalamin-loaded human MMUT converts (R)-methylmalonyl-CoA to succinyl-CoA in the coupled enzyme assay.

MCC converts 3-methylcrotonyl-CoA to 3-methylglutaconyl-CoA in the leucine breakdown pathway using biotin.

Human ACC1 uses biotin-dependent carboxylation of acetyl-CoA to generate malonyl-CoA.

Purified human ACC2 formed malonyl-CoA from acetyl-CoA in assays varying bicarbonate and ATP.

Acetyl-CoA stabilized human PC in a catalytically competent conformation in time-resolved structural and biochemical experiments.

Wild-type human CPT1B showed high-affinity malonyl-CoA binding and inhibition in recombinant mitochondrial assays.

Biotin uptake in human NCM460 cells was saturable, energy dependent and sodium dependent, with apparent Km 19.7 micromolar.

Pantothenic acid competitively inhibited biotin uptake in NCM460 cells, with Ki 14.4 micromolar.

PKC activators reduced biotin uptake in NCM460 cells; PKC inhibitors modestly increased uptake.

Chronic ethanol exposure reduced activity of both SLC5A6 promoters P1 and P2 in human Caco-2 cells.

Chronic ethanol feeding reduced carrier-mediated biotin uptake across rat jejunal brush-border and basolateral membranes.

Chronic ethanol exposure reduced carrier-mediated biotin uptake in human HK-2 cells.

Ethanol-exposed HK-2 cells showed reduced activity of the human SLC5A6 regulatory region.

Carbamazepine competitively inhibited biotin uptake in human intestinal brush-border vesicles (Ki 4.70 mmol/L), without inhibiting basolateral biotin transport.

Primidone competitively inhibited biotin uptake in human intestinal brush-border vesicles (Ki 2.25 mmol/L), without inhibiting basolateral biotin transport.

Urinary bisnorbiotin was higher in both carbamazepine/phenytoin-treated and phenobarbital-treated children than in controls.

The carbamazepine/phenytoin group had higher urinary 3-HIA, but only one child in that group had low urinary biotin.

Similar urinary recovery after the two larger oral biotin doses and the intravenous dose supported near-complete oral absorption in six healthy adults.

Biotin represented more than half of recovered urinary biotin-related material; bisnorbiotin, sulfoxide and other metabolites contributed the remainder.

Full-length human HLCS associated with the minimal biotin acceptor about twice as fast as the residue-58 isoform in pre-steady-state transfer measurements.

HLCS rapidly biotinylated the biotin-acceptor fragment of human PC, with transfer limited by enzyme-substrate association.

HLCS rapidly biotinylated the biotin-acceptor fragment of human PCCA, with transfer limited by enzyme-substrate association.

HLCS rapidly biotinylated the biotin-acceptor fragment of human MCCC1, with transfer limited by enzyme-substrate association.

HLCS biotinylation of the human ACACA acceptor fragment was relatively slow and depended hyperbolically on fragment concentration.

HLCS biotinylation of the human ACACB acceptor fragment was relatively slow and depended hyperbolically on fragment concentration.

The five affected children had serum biotinidase activity at 0–3% of the control mean, with combined carboxylase abnormalities.

Biotinidase impairment reduced carboxylase biotinylation and disrupted HLCS and carboxylase expression in the studied human cell model.

The human HLCS Gly581Ser variant had a biotin Km approximately 45 times the wild-type value.

The human HLCS Thr610-deletion variant had a biotin Km approximately three times the wild-type value.

Lower residual HLCS Vmax correlated with poorer PCC and clinical responses to biotin in the studied variants and patients; non-Km variants could also respond.

Newborn-screened children with biotinidase deficiency treated from early life and with good adherence generally had normal physical and cognitive development.

Acetyl-CoA-dependent stabilization of human PC triggered ATP hydrolysis and communication between its two reaction centers.

The human PC C-terminal structure displayed a conserved tetrameric arrangement, with a PC tetramerization domain identified by structural and mutagenesis analysis.

PCCA contains the biotin-carboxylase and biotin-carrier domains of human PCC.

PCCB provides the carboxyltransferase activity of human PCC.

Human PCC cryo-EM supported an alpha6-beta6 assembly similar to the bacterial holoenzyme architecture.

The human ACC1 biotin-carrier domain contains biotin covalently attached to Lys786.

Dephosphorylation and citrate treatment produced the activated human ACC1 filament state resolved by cryo-EM.

Citrate increased recombinant human ACC2 kcat and kcat/Km for ATP and acetyl-CoA.

In the studied human ACC2 domain, phosphorylated Ser222 occupied the putative dimer interface, disrupting polymerization and explaining AMPK-mediated inactivation.

Acacb-null mice had approximately 30-fold lower muscle malonyl-CoA and 10-fold lower heart malonyl-CoA than wild-type mice.

Soleus fatty-acid oxidation was about 30% higher in Acacb-null mice than in wild-type mice.

Deleting the first 28 residues of human CPT1B removed high-affinity malonyl-CoA binding and inhibition despite retained catalytic activity.

Active recombinant human MCC contained alpha and beta subunits at a one-to-one ratio.

Recombinant human MCC had an ATP Km of 45 ± 11 micromolar and a methylcrotonyl-CoA Km of 74 ± 7 micromolar.

Structural comparisons supported substrate-dependent, coordinated activation of human MCC.

Liver-specific Pcx deletion reduced hepatic anaplerosis, TCA-cycle intermediates and gluconeogenesis.

Liver-specific Pcx deletion depleted hepatic NADPH and worsened oxidative stress.

Liver-specific Pcx deletion depleted hepatic glutathione and was associated with greater oxidative stress and inflammation.

Liver-specific Pcx deletion depleted aspartate and impaired urea-cycle function, with hyperammonemia.

Genetic depletion of PC in human islets reduced glutathione and the GSH/GSSG ratio under nitrosative stress.

The experimental egg-white diet used avidin binding to reduce the availability of dietary biotin.

Urinary 3-HIA increased during 28-day biotin depletion in 11 adults; biotin-status indicators normalized in most after one week on a general diet.

Challenge-induced urinary 3-HIA rose more than twofold by day 14 in both biotin-depleted cohorts.

Challenge-induced urinary 3-hydroxyisovalerylcarnitine rose more than twofold by day 14 in both biotin-depleted cohorts.

Plasma 3-hydroxyisovalerylcarnitine was above the study reference interval in 7 of 10 adults by day 14 and 9 of 10 by day 28 of depletion, then fell with repletion.

Biotin-deficient but carnitine-sufficient HepG2 cells had more than tenfold higher intracellular 3-hydroxyisovalerylcarnitine than doubly sufficient cells.

Combined biotin and carnitine deficiency largely masked the increase in substrate-derived acylcarnitines observed with isolated biotin deficiency in HepG2 cells.

Carnitine repletion of doubly deficient HepG2 cells increased acetylcarnitine, propionylcarnitine and 3-hydroxyisovalerylcarnitine each by more than 50-fold.

At the controlled intake, pregnant women excreted 69% more 3-HIA than controls, while urinary 3-HIA-carnitine was 27% lower.

Lactating women excreted 76% more bisnorbiotin than controls, while 3-HIA and 3-HIA-carnitine excretion were lower.

Maternal biotin deprivation caused severe malformations in mice, no observed fetal malformations in rats, and high embryonic lethality in hamsters.

In the 88-person MCC-deficiency series, 57% were asymptomatic; 12 had acute metabolic decompensations, and genotype or biochemical phenotype did not reliably predict the course.

Premature twins on vitamin-limited parenteral nutrition developed severe illness associated with B2/B7 deficiency; the surviving twin improved after both vitamins were supplied.

Biotin-deficient human CD4 T cells secreted more IFN-gamma after anti-CD3/CD28 stimulation.

Biotin-deficient human CD4 T cells secreted more TNF after anti-CD3/CD28 stimulation.

Biotin-deficient human CD4 T cells secreted more IL-17 after anti-CD3/CD28 stimulation.

The study linked the heightened inflammatory response of biotin-deficient human CD4 T cells to enhanced mTOR-pathway activation.

LPS reduced the cell-surface fraction of SMVT in NCM460 cells without reducing total SMVT protein or RNA.

LPS reduced carrier-mediated biotin uptake in NCM460 cells; CK2 inhibition and a putative CK2-site SMVT mutant supported a CK2-related trafficking mechanism.

Vancomycin-associated L. murinus expansion consumed residual gut biotin in the mouse experiments.

Biotin restored hair in SPF mice with established alopecia after combined dietary deprivation and vancomycin-associated dysbiosis.