Biotin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

evidence_span

{"source_cache": "artifacts/chromium-research/17506119.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126", "start_char": 0, "end_char": 1739, "text_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126"}

experimental_model

Randomized double-blind placebo-controlled combination trial; 447 enrolled

exposure

600 µg Cr(III) as picolinate plus 2 mg biotin/day for 90 days with stable oral diabetes medication

limitations

There were no chromium-only or biotin-only arms. The design cannot identify the active ingredient or prove synergy. Baseline-HbA1c subgroup effects are separately limited.

nutrient_topic

Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium

organism

Human with poorly controlled type 2 diabetes

plain_language

The combination also improved fasting glucose in this trial.

primary_references

[chromium-p17506119] Chromium picolinate and biotin combination improves glucose metabolism in treated, uncontrolled overweight to obese patients with type 2 diabetes. (2008). https://pubmed.ncbi.nlm.nih.gov/17506119/ DOI: 10.1002/dmrr.755

tissue_or_cell_type

HbA1c and fasting glucose

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 705–716

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 combination trial; 447 enrolled · source_derived_draft · unverified_draft

### chromium-biotin-combination-glucose Fasting glucose changed by −9.8 mg/dL with chromium picolinate plus biotin versus +0.7 mg/dL with placebo (p=0.02). Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The combination also improved fasting glucose in this trial. organism: Human with poorly controlled type 2 diabetes tissue_or_cell_type: HbA1c and fasting glucose experimental_model: Randomized double-blind placebo-controlled combination trial; 447 enrolled limitations: There were no chromium-only or biotin-only arms. The design cannot identify the active ingredient or prove synergy. Baseline-HbA1c subgroup effects are separately limited. exposure: 600 µg Cr(III) as picolinate plus 2 mg biotin/day for 90 days with stable oral diabetes medication evidence_span: {"source_cache": "artifacts/chromium-research/17506119.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126", "start_char": 0, "end_char": 1739, "text_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126"} [chromium-p17506119] Chromium picolinate and biotin combination improves glucose metabolism in treated, uncontrolled overweight to obese patients with type 2 diabetes. (2008). https://pubmed.ncbi.nlm.nih.gov/17506119/ DOI: 10.1002/dmrr.755

evidence_span

{"source_cache": "artifacts/chromium-research/17506119.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126", "start_char": 0, "end_char": 1739, "text_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126"}

experimental_model

Randomized double-blind placebo-controlled combination trial; 447 enrolled

exposure

600 µg Cr(III) as picolinate plus 2 mg biotin/day for 90 days with stable oral diabetes medication

limitations

There were no chromium-only or biotin-only arms. The design cannot identify the active ingredient or prove synergy. Baseline-HbA1c subgroup effects are separately limited.

nutrient_topic

Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium

organism

Human with poorly controlled type 2 diabetes

plain_language

The two-ingredient treatment improved the average long-term glucose marker, but the contribution of each ingredient is unresolved.

primary_references

[chromium-p17506119] Chromium picolinate and biotin combination improves glucose metabolism in treated, uncontrolled overweight to obese patients with type 2 diabetes. (2008). https://pubmed.ncbi.nlm.nih.gov/17506119/ DOI: 10.1002/dmrr.755

tissue_or_cell_type

HbA1c and fasting glucose

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 692–703

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 combination trial; 447 enrolled · source_derived_draft · unverified_draft

### chromium-biotin-combination-hba1c The combination trial reported a between-group difference in HbA1c change (p=0.03); HbA1c fell 0.54 percentage points within the active-treatment group. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two-ingredient treatment improved the average long-term glucose marker, but the contribution of each ingredient is unresolved. organism: Human with poorly controlled type 2 diabetes tissue_or_cell_type: HbA1c and fasting glucose experimental_model: Randomized double-blind placebo-controlled combination trial; 447 enrolled limitations: There were no chromium-only or biotin-only arms. The design cannot identify the active ingredient or prove synergy. Baseline-HbA1c subgroup effects are separately limited. exposure: 600 µg Cr(III) as picolinate plus 2 mg biotin/day for 90 days with stable oral diabetes medication evidence_span: {"source_cache": "artifacts/chromium-research/17506119.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126", "start_char": 0, "end_char": 1739, "text_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126"} [chromium-p17506119] Chromium picolinate and biotin combination improves glucose metabolism in treated, uncontrolled overweight to obese patients with type 2 diabetes. (2008). https://pubmed.ncbi.nlm.nih.gov/17506119/ DOI: 10.1002/dmrr.755

evidence_span

{"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"}

experimental_model

Six-group high-fat-diet supplementation experiment

exposure

42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure

limitations

No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped.

nutrient_topic

Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium

organism

Male Sprague-Dawley rats

plain_language

This combination changed GLUT1 abundance in the rat experiment; the independent contribution of chromium was not isolated.

primary_references

[chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851

tissue_or_cell_type

Brain, liver and systemic metabolism

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 718–729

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-group high-fat-diet supplementation experiment · source_derived_draft · unverified_draft

### chromium-biotin-rat-glut1 The chromium-histidinate-plus-biotin condition gave the highest reported GLUT1 protein levels among the compared high-fat-diet interventions in brain and liver. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This combination changed GLUT1 abundance in the rat experiment; the independent contribution of chromium was not isolated. organism: Male Sprague-Dawley rats tissue_or_cell_type: Brain, liver and systemic metabolism experimental_model: Six-group high-fat-diet supplementation experiment limitations: No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped. exposure: 42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure evidence_span: {"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"} [chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851

evidence_span

{"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"}

experimental_model

Six-group high-fat-diet supplementation experiment

exposure

42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure

limitations

No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped.

nutrient_topic

Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium

organism

Male Sprague-Dawley rats

plain_language

This combination changed GLUT3 abundance in the rat experiment; the independent contribution of chromium was not isolated.

primary_references

[chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851

tissue_or_cell_type

Brain, liver and systemic metabolism

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 731–742

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-group high-fat-diet supplementation experiment · source_derived_draft · unverified_draft

### chromium-biotin-rat-glut3 The chromium-histidinate-plus-biotin condition gave the highest reported GLUT3 protein levels among the compared high-fat-diet interventions in brain and liver. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This combination changed GLUT3 abundance in the rat experiment; the independent contribution of chromium was not isolated. organism: Male Sprague-Dawley rats tissue_or_cell_type: Brain, liver and systemic metabolism experimental_model: Six-group high-fat-diet supplementation experiment limitations: No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped. exposure: 42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure evidence_span: {"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"} [chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851

evidence_span

{"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"}

experimental_model

Six-group high-fat-diet supplementation experiment

exposure

42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure

limitations

No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped.

nutrient_topic

Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium

organism

Male Sprague-Dawley rats

plain_language

This combination changed IRS-1 abundance in the rat experiment; the independent contribution of chromium was not isolated.

primary_references

[chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851

tissue_or_cell_type

Brain, liver and systemic metabolism

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 744–755

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-group high-fat-diet supplementation experiment · source_derived_draft · unverified_draft

### chromium-biotin-rat-irs1 The chromium-histidinate-plus-biotin condition gave the highest reported IRS-1 protein levels among the compared high-fat-diet interventions in brain and liver. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This combination changed IRS-1 abundance in the rat experiment; the independent contribution of chromium was not isolated. organism: Male Sprague-Dawley rats tissue_or_cell_type: Brain, liver and systemic metabolism experimental_model: Six-group high-fat-diet supplementation experiment limitations: No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped. exposure: 42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure evidence_span: {"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"} [chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851

evidence_span

{"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"}

experimental_model

Six-group high-fat-diet supplementation experiment

exposure

42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure

limitations

No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped.

nutrient_topic

Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium

organism

Male Sprague-Dawley rats

plain_language

This combination changed PPAR-gamma abundance in the rat experiment; the independent contribution of chromium was not isolated.

primary_references

[chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851

tissue_or_cell_type

Brain, liver and systemic metabolism

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 757–768

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-group high-fat-diet supplementation experiment · source_derived_draft · unverified_draft

### chromium-biotin-rat-pparg The chromium-histidinate-plus-biotin condition gave the highest reported PPAR-gamma protein levels among the compared high-fat-diet interventions in brain and liver. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This combination changed PPAR-gamma abundance in the rat experiment; the independent contribution of chromium was not isolated. organism: Male Sprague-Dawley rats tissue_or_cell_type: Brain, liver and systemic metabolism experimental_model: Six-group high-fat-diet supplementation experiment limitations: No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped. exposure: 42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure evidence_span: {"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"} [chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851

evidence_access

Primary full text

experimental_model

Fly feeding; grape extract, with separate piceid body-fat experiments.

limitations

Not purified resveratrol exposure; reduced fly fat was not explained by lost carboxylase biotinylation.

nutrient_topic

Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol

plain_language

Compensatory expression can reverse an isolated-enzyme prediction.

primary_references

Resveratrol compounds inhibit human holocarboxylase synthetase and cause a lean phenotype in Drosophila melanogaster. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26303405/ · DOI 10.1016/j.jnutbio.2015.07.004

Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 358–364

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Fly feeding; grape extract, with separate piceid body-fat experiments. · source_derived_draft · unverified_draft

## resveratrol-fly-compensation Compensatory expression can reverse an isolated-enzyme prediction. Grape-leaf feeding increased HLCS protein and biotinylated carboxylases in Drosophila brummer mutants despite the extract inhibiting human HLCS in vitro. Model: Fly feeding; grape extract, with separate piceid body-fat experiments. Limitations: Not purified resveratrol exposure; reduced fly fat was not explained by lost carboxylase biotinylation. Evidence access: Primary full text Resveratrol compounds inhibit human holocarboxylase synthetase and cause a lean phenotype in Drosophila melanogaster. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26303405/ · DOI 10.1016/j.jnutbio.2015.07.004

evidence_access

Primary full text

experimental_model

Gel-based biotin-acceptor assay and dose response.

limitations

Human biotin depletion or failure of biotin repletion was not demonstrated.

nutrient_topic

Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol

plain_language

A direct laboratory connection to biotin activation is searchable.

primary_references

Resveratrol compounds inhibit human holocarboxylase synthetase and cause a lean phenotype in Drosophila melanogaster. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26303405/ · DOI 10.1016/j.jnutbio.2015.07.004

Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 342–348

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Gel-based biotin-acceptor assay and dose response. · source_derived_draft · unverified_draft

## resveratrol-hlcs-inhibition A direct laboratory connection to biotin activation is searchable. Resveratrol inhibited recombinant human HLCS-dependent biotinylation in vitro, with reported IC50 approximately 3.70 micromolar. Model: Gel-based biotin-acceptor assay and dose response. Limitations: Human biotin depletion or failure of biotin repletion was not demonstrated. Evidence access: Primary full text Resveratrol compounds inhibit human holocarboxylase synthetase and cause a lean phenotype in Drosophila melanogaster. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26303405/ · DOI 10.1016/j.jnutbio.2015.07.004

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

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

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

cross_nutrient

true

experimental_model

Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells

exposure

Antibody-free membrane-localization method, with human/monkey microvessel proteomics and human expression analyses.

limitations

Abstract does not resolve which species supplied every localization preparation. The result addresses blood-facing localization, not the unidentified abluminal export step.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens and monkey microvessel preparations; localization sample allocation not detailed in abstract

plain_language

Brain capillary SMVT is concentrated on the side facing the blood.

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

Brain capillary endothelium

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 301–312

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-luminal-localization The brain-microvessel study localized SLC5A6 preferentially to the luminal membrane of brain capillary endothelium. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Brain capillary SMVT is concentrated on the side facing the blood. organism: Homo sapiens and monkey microvessel preparations; localization sample allocation not detailed in abstract tissue_or_cell_type: Brain capillary endothelium experimental_model: Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells limitations: Abstract does not resolve which species supplied every localization preparation. The result addresses blood-facing localization, not the unidentified abluminal export step. exposure: Antibody-free membrane-localization method, with human/monkey microvessel proteomics and human expression analyses. 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

cross_nutrient

true

experimental_model

Functional human SMVT-GFP expression and imaging in polarized renal and intestinal epithelial cell lines

exposure

Full-length human SMVT-GFP expression and polarized membrane imaging.

limitations

Abstract-only; fluorescent fusion-protein localization in cell lines is not a measurement of net intestinal pantothenate absorption. The abstract does not name the intestinal cell line.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens (transporter); expression-host species not specified in the retrieved abstract

plain_language

In the intestinal cell models, SMVT sits on the surface facing the intestinal contents.

primary_references

[b5-trans-targeting2009] Membrane targeting and intracellular trafficking of the human sodium-dependent multivitamin transporter in polarized epithelial cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19211916/ DOI: 10.1152/ajpcell.00396.2008

tissue_or_cell_type

Polarized intestinal epithelial cell model

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 223–234

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Functional human SMVT-GFP expression and imaging in polarized renal and intestinal epithelial cell lines · source_derived_draft · unverified_draft

### b5-trans-epithelial-apical-targeting Functional full-length human SMVT-GFP localized to the apical membrane in the studied polarized intestinal epithelial cell lines. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: In the intestinal cell models, SMVT sits on the surface facing the intestinal contents. organism: Homo sapiens (transporter); expression-host species not specified in the retrieved abstract tissue_or_cell_type: Polarized intestinal epithelial cell model experimental_model: Functional human SMVT-GFP expression and imaging in polarized renal and intestinal epithelial cell lines limitations: Abstract-only; fluorescent fusion-protein localization in cell lines is not a measurement of net intestinal pantothenate absorption. The abstract does not name the intestinal cell line. exposure: Full-length human SMVT-GFP expression and polarized membrane imaging. cross_nutrient: true [b5-trans-targeting2009] Membrane targeting and intracellular trafficking of the human sodium-dependent multivitamin transporter in polarized epithelial cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19211916/ DOI: 10.1152/ajpcell.00396.2008

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

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

cross_nutrient

true

experimental_model

Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells

exposure

3.7-angstrom cryo-EM pantothenate complex; molecular-dynamics support for the binding model.

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. Atom-level interactions are structural-model interpretations; no specific dietary threshold follows.

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 anchors the charged end of B5 through specific contacts in its binding pocket.

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 ligand-binding pocket

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 418–429

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-carboxyl-recognition In the human SMVT–pantothenate structural model, the substrate carboxyl group interacts with backbone amino groups of Ser81/Ala84 and hydrogen-bonds to Tyr156. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT anchors the charged end of B5 through specific contacts in its binding pocket. organism: Homo sapiens tissue_or_cell_type: Purified human SMVT ligand-binding pocket 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. Atom-level interactions are structural-model interpretations; no specific dietary threshold follows. exposure: 3.7-angstrom cryo-EM pantothenate complex; molecular-dynamics support for the binding model. 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

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

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

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

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

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

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

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

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