Component
D-Galactose
D-Galactose. Experimental scope belongs to each linked claim.
6 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
Oral galactose improved transferrin glycoform patterns and reduced hypogalactosylated serum N-glycans in the two TMEM165-CDG patients.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Human TMEM165 deficiency (underlying_defect)
- evidence_span
- {"source_cache": "artifacts/manganese-clinical-sources/tmem165patients.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "3899c8a8d58b702858b7e1e74723d46a9825f4d7846b969ccf33db688fa16eac", "start_char": 0, "end_char": 2039, "text_sha256": "3899c8a8d58b702858b7e1e74723d46a9825f4d7846b969ccf33db688fa16eac", "text_characters": 2039}
- experimental_model
- Two unrelated patients with TMEM165-CDG
- exposure
- Oral D-galactose; indexed abstract reports 1 g/kg/day in individuals homozygous for c.792+182G>A.
- limitations
- Primary abstract used for these claims; this nominal amount is not a reconstruction of the full titration schedule. Cell manganese-rescue experiments in the same paper must not be recast as manganese treatment of the patients.
- nutrient_topic
- Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
- organism
- Homo sapiens
- plain_language
- Galactose improved selected blood sugar-chain markers despite the genetic defect.
- primary_references
- [mn-clin-tmem165patients] Galactose Supplementation in Patients With TMEM165-CDG Rescues the Glycosylation Defects. (2017). https://pubmed.ncbi.nlm.nih.gov/28323990/ DOI: 10.1210/jc.2016-3443
- tissue_or_cell_type
- Serum glycosylation
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 1244–1256
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two unrelated patients with TMEM165-CDG · source_derived_draft · unverified_draft
### mn-clin-tmem165-gal-patients Oral galactose improved transferrin glycoform patterns and reduced hypogalactosylated serum N-glycans in the two TMEM165-CDG patients. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Galactose improved selected blood sugar-chain markers despite the genetic defect. organism: Homo sapiens tissue_or_cell_type: Serum glycosylation experimental_model: Two unrelated patients with TMEM165-CDG limitations: Primary abstract used for these claims; this nominal amount is not a reconstruction of the full titration schedule. Cell manganese-rescue experiments in the same paper must not be recast as manganese treatment of the patients. exposure: Oral D-galactose; indexed abstract reports 1 g/kg/day in individuals homozygous for c.792+182G>A. cross_nutrient: Human TMEM165 deficiency (underlying_defect) evidence_span: {"source_cache": "artifacts/manganese-clinical-sources/tmem165patients.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "3899c8a8d58b702858b7e1e74723d46a9825f4d7846b969ccf33db688fa16eac", "start_char": 0, "end_char": 2039, "text_sha256": "3899c8a8d58b702858b7e1e74723d46a9825f4d7846b969ccf33db688fa16eac", "text_characters": 2039} [mn-clin-tmem165patients] Galactose Supplementation in Patients With TMEM165-CDG Rescues the Glycosylation Defects. (2017). https://pubmed.ncbi.nlm.nih.gov/28323990/ DOI: 10.1210/jc.2016-3443
Complete structured claim and evidenceD-galactose did not rescue the decorin glycosaminoglycan defect in the tested mouse Tmem165-knockout ATDC5 cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Mouse TMEM165 (affected_protein)
- evidence_span
- {"source_cache": "artifacts/manganese-glycosylation-sources/morelle2022.txt", "locator": "Results and Figure 5; decorin", "file_sha256": "91d05677c6d7bb4224f71742888e39533e3f130d59e6b2ffcae3e2b2c058e9aa", "start_char": 25939, "end_char": 27086, "text_sha256": "d94138936b018635104317fedba6c1298f0d54c6cd7b3f578b60000cea925bf5", "text_characters": 1147}
- experimental_model
- Tmem165-knockout mouse ATDC5 chondrogenic cells
- exposure
- Decorin-transfected ATDC5 cells: 1 micromolar MnCl2, 1 millimolar galactose or 1 millimolar xylose for 36 hours.
- limitations
- Decorin chondroitin-sulfate elongation in mouse chondrogenic cells. This is a separate model from the human HEK N/O-glycosylation assays and does not establish clinical cartilage rescue.
- nutrient_topic
- Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
- organism
- Mus musculus
- plain_language
- Improved N-glycosylation did not mean the proteoglycan defect was corrected.
- primary_references
- [mn-gly-morelle2022] Differential Effects of D-Galactose Supplementation on Golgi Glycosylation Defects in TMEM165 Deficiency. (2022). https://pubmed.ncbi.nlm.nih.gov/35693943/ DOI: 10.3389/fcell.2022.903953
- tissue_or_cell_type
- Mouse chondrogenic ATDC5 cells and secreted decorin
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 824–836
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Tmem165-knockout mouse ATDC5 chondrogenic cells · source_derived_draft · unverified_draft
### mn-gly-gal-gag-null D-galactose did not rescue the decorin glycosaminoglycan defect in the tested mouse Tmem165-knockout ATDC5 cells. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Improved N-glycosylation did not mean the proteoglycan defect was corrected. organism: Mus musculus tissue_or_cell_type: Mouse chondrogenic ATDC5 cells and secreted decorin experimental_model: Tmem165-knockout mouse ATDC5 chondrogenic cells limitations: Decorin chondroitin-sulfate elongation in mouse chondrogenic cells. This is a separate model from the human HEK N/O-glycosylation assays and does not establish clinical cartilage rescue. exposure: Decorin-transfected ATDC5 cells: 1 micromolar MnCl2, 1 millimolar galactose or 1 millimolar xylose for 36 hours. cross_nutrient: Mouse TMEM165 (affected_protein) evidence_span: {"source_cache": "artifacts/manganese-glycosylation-sources/morelle2022.txt", "locator": "Results and Figure 5; decorin", "file_sha256": "91d05677c6d7bb4224f71742888e39533e3f130d59e6b2ffcae3e2b2c058e9aa", "start_char": 25939, "end_char": 27086, "text_sha256": "d94138936b018635104317fedba6c1298f0d54c6cd7b3f578b60000cea925bf5", "text_characters": 1147} [mn-gly-morelle2022] Differential Effects of D-Galactose Supplementation on Golgi Glycosylation Defects in TMEM165 Deficiency. (2022). https://pubmed.ncbi.nlm.nih.gov/35693943/ DOI: 10.3389/fcell.2022.903953
Complete structured claim and evidenceD-galactose improved LAMP2 N-glycosylation only partially across the tested concentrations and times; the authors attributed residual underglycosylated protein to slow turnover.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Lysosome-associated membrane glycoprotein 2 (measured_protein); TMEM165 Golgi cation-homeostasis protein (affected_protein); UDP-galactose (related_donor)
- evidence_span
- {"source_cache": "artifacts/manganese-glycosylation-sources/morelle2022.txt", "locator": "Results and Figure 1; LAMP2 subset recovery", "file_sha256": "91d05677c6d7bb4224f71742888e39533e3f130d59e6b2ffcae3e2b2c058e9aa", "start_char": 15482, "end_char": 17574, "text_sha256": "b7ffb42fc1d2094bd301171da36864a49f430e69b184ef0594b392c6ac7802dd", "text_characters": 2092}
- experimental_model
- Control and TMEM165-knockout HEK293 glycosylation assays
- exposure
- Figure 1: 1 micromolar MnCl2 for 8, 16 or 24 hours; galactose dose/time comparisons include 1 and 2.5 millimolar and 24–72 hours.
- limitations
- Cell rescue is not evidence for a safe human dose. N-linked, mucin-type O-linked and proteoglycan GAG endpoints are distinct; restoring one is not proof of global correction.
- nutrient_topic
- Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
- organism
- Homo sapiens
- plain_language
- Providing the sugar helped this readout, but some abnormal forms persisted throughout the tested conditions.
- primary_references
- [mn-gly-morelle2022] Differential Effects of D-Galactose Supplementation on Golgi Glycosylation Defects in TMEM165 Deficiency. (2022). https://pubmed.ncbi.nlm.nih.gov/35693943/ DOI: 10.3389/fcell.2022.903953
- tissue_or_cell_type
- HEK293 cells and secretory glycoproteins
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 796–808
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Control and TMEM165-knockout HEK293 glycosylation assays · source_derived_draft · unverified_draft
### mn-gly-gal-n-linked-rescue D-galactose improved LAMP2 N-glycosylation only partially across the tested concentrations and times; the authors attributed residual underglycosylated protein to slow turnover. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Providing the sugar helped this readout, but some abnormal forms persisted throughout the tested conditions. organism: Homo sapiens tissue_or_cell_type: HEK293 cells and secretory glycoproteins experimental_model: Control and TMEM165-knockout HEK293 glycosylation assays limitations: Cell rescue is not evidence for a safe human dose. N-linked, mucin-type O-linked and proteoglycan GAG endpoints are distinct; restoring one is not proof of global correction. exposure: Figure 1: 1 micromolar MnCl2 for 8, 16 or 24 hours; galactose dose/time comparisons include 1 and 2.5 millimolar and 24–72 hours. cross_nutrient: Lysosome-associated membrane glycoprotein 2 (measured_protein); TMEM165 Golgi cation-homeostasis protein (affected_protein); UDP-galactose (related_donor) evidence_span: {"source_cache": "artifacts/manganese-glycosylation-sources/morelle2022.txt", "locator": "Results and Figure 1; LAMP2 subset recovery", "file_sha256": "91d05677c6d7bb4224f71742888e39533e3f130d59e6b2ffcae3e2b2c058e9aa", "start_char": 15482, "end_char": 17574, "text_sha256": "b7ffb42fc1d2094bd301171da36864a49f430e69b184ef0594b392c6ac7802dd", "text_characters": 2092} [mn-gly-morelle2022] Differential Effects of D-Galactose Supplementation on Golgi Glycosylation Defects in TMEM165 Deficiency. (2022). https://pubmed.ncbi.nlm.nih.gov/35693943/ DOI: 10.3389/fcell.2022.903953
Complete structured claim and evidenceD-galactose partially improved the 24-hour O-glycan lectin readout but failed to rescue the three-day benzyl-GalNAc mass-spectrometry phenotype in TMEM165-knockout HEK cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- TMEM165 Golgi cation-homeostasis protein (affected_protein); Manganese(II) ion (effective_comparator)
- evidence_span
- {"source_cache": "artifacts/manganese-glycosylation-sources/morelle2022.txt", "locator": "Results; O-linked lectin and mass-spectrometry endpoints", "file_sha256": "91d05677c6d7bb4224f71742888e39533e3f130d59e6b2ffcae3e2b2c058e9aa", "start_char": 19358, "end_char": 22255, "text_sha256": "e0b72a5427217107308f73e2304f47c761a25448096f516ca75c497eb8e389d5", "text_characters": 2897}
- experimental_model
- Control and TMEM165-knockout HEK293 glycosylation assays
- exposure
- Figure 3 lectin staining: 2.5 micromolar MnCl2 and/or 1 millimolar galactose for 24 hours. Figure 4: same additions with 250 micromolar benzyl-GalNAc for three days.
- limitations
- Cell rescue is not evidence for a safe human dose. N-linked, mucin-type O-linked and proteoglycan GAG endpoints are distinct; restoring one is not proof of global correction.
- nutrient_topic
- Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
- organism
- Homo sapiens
- plain_language
- One O-glycan test improved partly while a different test remained abnormal; galactose did not normalize this pathway.
- primary_references
- [mn-gly-morelle2022] Differential Effects of D-Galactose Supplementation on Golgi Glycosylation Defects in TMEM165 Deficiency. (2022). https://pubmed.ncbi.nlm.nih.gov/35693943/ DOI: 10.3389/fcell.2022.903953
- tissue_or_cell_type
- HEK293 cells and secretory glycoproteins
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 810–822
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Control and TMEM165-knockout HEK293 glycosylation assays · source_derived_draft · unverified_draft
### mn-gly-gal-o-linked-limited D-galactose partially improved the 24-hour O-glycan lectin readout but failed to rescue the three-day benzyl-GalNAc mass-spectrometry phenotype in TMEM165-knockout HEK cells. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: One O-glycan test improved partly while a different test remained abnormal; galactose did not normalize this pathway. organism: Homo sapiens tissue_or_cell_type: HEK293 cells and secretory glycoproteins experimental_model: Control and TMEM165-knockout HEK293 glycosylation assays limitations: Cell rescue is not evidence for a safe human dose. N-linked, mucin-type O-linked and proteoglycan GAG endpoints are distinct; restoring one is not proof of global correction. exposure: Figure 3 lectin staining: 2.5 micromolar MnCl2 and/or 1 millimolar galactose for 24 hours. Figure 4: same additions with 250 micromolar benzyl-GalNAc for three days. cross_nutrient: TMEM165 Golgi cation-homeostasis protein (affected_protein); Manganese(II) ion (effective_comparator) evidence_span: {"source_cache": "artifacts/manganese-glycosylation-sources/morelle2022.txt", "locator": "Results; O-linked lectin and mass-spectrometry endpoints", "file_sha256": "91d05677c6d7bb4224f71742888e39533e3f130d59e6b2ffcae3e2b2c058e9aa", "start_char": 19358, "end_char": 22255, "text_sha256": "e0b72a5427217107308f73e2304f47c761a25448096f516ca75c497eb8e389d5", "text_characters": 2897} [mn-gly-morelle2022] Differential Effects of D-Galactose Supplementation on Golgi Glycosylation Defects in TMEM165 Deficiency. (2022). https://pubmed.ncbi.nlm.nih.gov/35693943/ DOI: 10.3389/fcell.2022.903953
Complete structured claim and evidence
Where it participates (unsigned role)
Galactose plus uridine improved patient 2’s transferrin isoform pattern within 14 days.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- D-Galactose (coadministered_substrate); Uridine (coadministered_substrate); Human ZIP8 (SLC39A8) (affected_protein)
- evidence_span
- {"source_cache": "artifacts/manganese-clinical-sources/riley2017.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "31e4e33ec5601d443fb2d469b2e2c7d1fd89c611db0f41938b43007952d0f005", "start_char": 0, "end_char": 1732, "text_sha256": "31e4e33ec5601d443fb2d469b2e2c7d1fd89c611db0f41938b43007952d0f005", "text_characters": 1732}
- experimental_model
- Two sisters with homozygous SLC39A8 p.Cys113Ser
- exposure
- Respiratory-chain tests in patient 1; manganese and transferrin measurements and galactose-plus-uridine response in patient 2.
- limitations
- Measurements were not performed in both sisters interchangeably. The proposed SOD2 explanation was not directly demonstrated; manganese had only recently been added and cannot explain the already observed 14-day galactose/uridine response.
- nutrient_topic
- Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
- organism
- Homo sapiens
- plain_language
- A combined substrate-support treatment improved the measured sugar pattern.
- primary_references
- [mn-clin-riley2017] A SLC39A8 variant causes manganese deficiency, and glycosylation and mitochondrial disorders. (2017). https://pubmed.ncbi.nlm.nih.gov/27995398/ DOI: 10.1007/s10545-016-0010-6
- tissue_or_cell_type
- Patient-specific liver, muscle and blood measurements
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 1230–1242
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two sisters with homozygous SLC39A8 p.Cys113Ser · source_derived_draft · unverified_draft
### mn-clin-zip8-gal-uridine Galactose plus uridine improved patient 2’s transferrin isoform pattern within 14 days. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: A combined substrate-support treatment improved the measured sugar pattern. organism: Homo sapiens tissue_or_cell_type: Patient-specific liver, muscle and blood measurements experimental_model: Two sisters with homozygous SLC39A8 p.Cys113Ser limitations: Measurements were not performed in both sisters interchangeably. The proposed SOD2 explanation was not directly demonstrated; manganese had only recently been added and cannot explain the already observed 14-day galactose/uridine response. exposure: Respiratory-chain tests in patient 1; manganese and transferrin measurements and galactose-plus-uridine response in patient 2. cross_nutrient: D-Galactose (coadministered_substrate); Uridine (coadministered_substrate); Human ZIP8 (SLC39A8) (affected_protein) evidence_span: {"source_cache": "artifacts/manganese-clinical-sources/riley2017.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "31e4e33ec5601d443fb2d469b2e2c7d1fd89c611db0f41938b43007952d0f005", "start_char": 0, "end_char": 1732, "text_sha256": "31e4e33ec5601d443fb2d469b2e2c7d1fd89c611db0f41938b43007952d0f005", "text_characters": 1732} [mn-clin-riley2017] A SLC39A8 variant causes manganese deficiency, and glycosylation and mitochondrial disorders. (2017). https://pubmed.ncbi.nlm.nih.gov/27995398/ DOI: 10.1007/s10545-016-0010-6
Complete structured claim and evidenceWith serum lot 4, combining 1 micromolar manganese and 1 millimolar galactose restored fully glycosylated LAMP2 more effectively than either alone.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Manganese(II) ion (combined_ion); D-Galactose (combined_sugar); TMEM165 Golgi cation-homeostasis protein (affected_protein)
- evidence_span
- {"source_cache": "artifacts/manganese-glycosylation-sources/serum2020.txt", "locator": "Results and Figure 9; use 1 mM galactose from setup and legend, rather than the subsequent prose unit typo", "file_sha256": "203365df4c837f50483da9ec16cb0882674cf4903bbda21aa7374205d72ade69", "start_char": 9804, "end_char": 10848, "text_sha256": "3547ececbb7198f699bd64bcd033276f18a8e3d3b7c02c4f907f25a267444bec", "text_characters": 1044}
- experimental_model
- TMEM165-knockout HEK cell cultures with different fetal bovine serum lots
- exposure
- Serum lot 4; 1 micromolar manganese, 1 millimolar galactose or both for 24 hours.
- limitations
- Serum manganese contributes to the result but is not the sole determinant. These are medium concentrations, not blood thresholds or supplementation regimens.
- nutrient_topic
- Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
- organism
- Homo sapiens
- plain_language
- A combined supply improved a result that responded poorly to either component alone.
- primary_references
- [mn-gly-serum2020] Fetal bovine serum impacts the observed N-glycosylation defects in TMEM165 KO HEK cells. (2020). https://pubmed.ncbi.nlm.nih.gov/31415112/ DOI: 10.1002/jimd.12161
- tissue_or_cell_type
- Golgi glycosylation in HEK cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 866–878
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · TMEM165-knockout HEK cell cultures with different fetal bovine serum lots · source_derived_draft · unverified_draft
### mn-gly-gal-mn-combination With serum lot 4, combining 1 micromolar manganese and 1 millimolar galactose restored fully glycosylated LAMP2 more effectively than either alone. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: A combined supply improved a result that responded poorly to either component alone. organism: Homo sapiens tissue_or_cell_type: Golgi glycosylation in HEK cells experimental_model: TMEM165-knockout HEK cell cultures with different fetal bovine serum lots limitations: Serum manganese contributes to the result but is not the sole determinant. These are medium concentrations, not blood thresholds or supplementation regimens. exposure: Serum lot 4; 1 micromolar manganese, 1 millimolar galactose or both for 24 hours. cross_nutrient: Manganese(II) ion (combined_ion); D-Galactose (combined_sugar); TMEM165 Golgi cation-homeostasis protein (affected_protein) evidence_span: {"source_cache": "artifacts/manganese-glycosylation-sources/serum2020.txt", "locator": "Results and Figure 9; use 1 mM galactose from setup and legend, rather than the subsequent prose unit typo", "file_sha256": "203365df4c837f50483da9ec16cb0882674cf4903bbda21aa7374205d72ade69", "start_char": 9804, "end_char": 10848, "text_sha256": "3547ececbb7198f699bd64bcd033276f18a8e3d3b7c02c4f907f25a267444bec", "text_characters": 1044} [mn-gly-serum2020] Fetal bovine serum impacts the observed N-glycosylation defects in TMEM165 KO HEK cells. (2020). https://pubmed.ncbi.nlm.nih.gov/31415112/ DOI: 10.1002/jimd.12161
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.