Component

Glycine cleavage flux

Independently recorded entity or measured process. Linked claims specify compartment, assay and experimental scope.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What acts on it

  1. Restriction did not significantly change glycine cleavage or serine synthesis from GCS-derived one-carbon units.

    Vitamin B6 → Glycine cleavage flux source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    B6-dependent glycine cleavage supplies folate one-carbon chemistry.
    experimental_model
    Thirteen healthy adults (seven men, six women; ages 20–39); glycine and leucine stable-isotope infusion.
    exposure
    Moderate dietary B6 restriction; plasma PLP55±4 to 23±1 nmol/L.
    limitations
    Whole-body kinetics do not resolve separate organs or prove severe deficiency harmless.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    This folate-linked carbon supply remained measurable despite lower blood B6.
    primary_references
    [b6-lamers2009] Moderate dietary vitamin B-6 restriction raises plasma glycine and cystathionine concentrations while minimally affecting the rates of glycine turnover and glycine cleavage in healthy men and women (2009). https://pubmed.ncbi.nlm.nih.gov/19158217/ DOI: 10.3945/jn.108.099184
    tissue_or_cell_type
    Human blood and whole-body measurements
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1397–1408

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Thirteen healthy adults (seven men, six women; ages 20–39); glycine and leucine stable-isotope infusion. · source_derived_draft · unverified_draft

    ### b6-glycine-cleavage-resilience Restriction did not significantly change glycine cleavage or serine synthesis from GCS-derived one-carbon units. Condition category: nutrient_deficiency nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: This folate-linked carbon supply remained measurable despite lower blood B6. organism: Homo sapiens tissue_or_cell_type: Human blood and whole-body measurements experimental_model: Thirteen healthy adults (seven men, six women; ages 20–39); glycine and leucine stable-isotope infusion. limitations: Whole-body kinetics do not resolve separate organs or prove severe deficiency harmless. exposure: Moderate dietary B6 restriction; plasma PLP55±4 to 23±1 nmol/L. cross_nutrient: B6-dependent glycine cleavage supplies folate one-carbon chemistry. [b6-lamers2009] Moderate dietary vitamin B-6 restriction raises plasma glycine and cystathionine concentrations while minimally affecting the rates of glycine turnover and glycine cleavage in healthy men and women (2009). https://pubmed.ncbi.nlm.nih.gov/19158217/ DOI: 10.3945/jn.108.099184
    Complete structured claim and evidence

  2. Despite LIPT1 deficiency, H-protein lipoylation, glycine-cleavage activity and glycine concentrations were normal in this case.

    Human lipoyl amidotransferase / LIPT1 → Glycine cleavage flux source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/ala-research/24256811.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57599dd35c58b21d16f2a5955ea667ec8211ab129ee7d0b639b31f18f0976eb2", "start_char": 0, "end_char": 1749, "text_sha256": "57599dd35c58b21d16f2a5955ea667ec8211ab129ee7d0b639b31f18f0976eb2"}
    experimental_model
    Affected patient, biochemical testing and complementation
    exposure
    Compound-heterozygous LIPT1 variants
    limitations
    Single rare inherited case; enzyme deficits are not interchangeable with nutritional deficiency.
    nutrient_topic
    Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. · Lipoic acid
    organism
    Human
    plain_language
    The glycine pathway can keep working when a later transfer step fails.
    primary_references
    [ala-p24256811] Mutations in the lipoyltransferase LIPT1 gene cause a fatal disease associated with a specific lipoylation defect of the 2-ketoacid dehydrogenase complexes. (2014). https://pubmed.ncbi.nlm.nih.gov/24256811/ DOI: 10.1093/hmg/ddt585
    tissue_or_cell_type
    Patient-derived cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Alpha-lipoic acid: cofactor assembly, redox signaling 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 · Affected patient, biochemical testing and complementation · source_derived_draft · unverified_draft

    ### ala-lipt1-glycine-spared Despite LIPT1 deficiency, H-protein lipoylation, glycine-cleavage activity and glycine concentrations were normal in this case. Condition category: machinery_impairment nutrient_topic: Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The glycine pathway can keep working when a later transfer step fails. organism: Human tissue_or_cell_type: Patient-derived cells experimental_model: Affected patient, biochemical testing and complementation limitations: Single rare inherited case; enzyme deficits are not interchangeable with nutritional deficiency. exposure: Compound-heterozygous LIPT1 variants evidence_span: {"source_cache": "artifacts/ala-research/24256811.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57599dd35c58b21d16f2a5955ea667ec8211ab129ee7d0b639b31f18f0976eb2", "start_char": 0, "end_char": 1749, "text_sha256": "57599dd35c58b21d16f2a5955ea667ec8211ab129ee7d0b639b31f18f0976eb2"} [ala-p24256811] Mutations in the lipoyltransferase LIPT1 gene cause a fatal disease associated with a specific lipoylation defect of the 2-ketoacid dehydrogenase complexes. (2014). https://pubmed.ncbi.nlm.nih.gov/24256811/ DOI: 10.1093/hmg/ddt585
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. GLRX5-associated cases showed deficient protein lipoylation and glycine-cleavage activity with elevated glycine.

    Human mitochondrial glutaredoxin 5 / GLRX5 → Glycine accumulation in lipoylation disorders source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/ala-research/24334290.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2d6f134f9da5ac532fac9c58757e80a0b51c9912f8ddbec39eb81d1e81ccbfb2", "start_char": 0, "end_char": 2342, "text_sha256": "2d6f134f9da5ac532fac9c58757e80a0b51c9912f8ddbec39eb81d1e81ccbfb2"}
    experimental_model
    Variant nonketotic hyperglycinemia cohort and cell complementation
    exposure
    LIAS, BOLA3 or GLRX5 variants; lipoate and mitochondrially targeted lipoate in cells
    limitations
    Phenotypes varied; respiratory-chain function was preserved in this series, unlike some other Fe-S disorders.
    nutrient_topic
    Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. · Lipoic acid
    organism
    Human
    plain_language
    A cofactor-assembly defect can mimic a defect in the glycine-cleavage enzymes themselves.
    primary_references
    [ala-p24334290] Variant non ketotic hyperglycinemia is caused by mutations in LIAS, BOLA3 and the novel gene GLRX5. (2014). https://pubmed.ncbi.nlm.nih.gov/24334290/ DOI: 10.1093/brain/awt328
    tissue_or_cell_type
    Eight genetically explained patients within an eleven-person group
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Alpha-lipoic acid: cofactor assembly, redox signaling 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 · Variant nonketotic hyperglycinemia cohort and cell complementation · source_derived_draft · unverified_draft

    ### ala-glrx5-glycine-failure GLRX5-associated cases showed deficient protein lipoylation and glycine-cleavage activity with elevated glycine. Condition category: machinery_impairment nutrient_topic: Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: A cofactor-assembly defect can mimic a defect in the glycine-cleavage enzymes themselves. organism: Human tissue_or_cell_type: Eight genetically explained patients within an eleven-person group experimental_model: Variant nonketotic hyperglycinemia cohort and cell complementation limitations: Phenotypes varied; respiratory-chain function was preserved in this series, unlike some other Fe-S disorders. exposure: LIAS, BOLA3 or GLRX5 variants; lipoate and mitochondrially targeted lipoate in cells evidence_span: {"source_cache": "artifacts/ala-research/24334290.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2d6f134f9da5ac532fac9c58757e80a0b51c9912f8ddbec39eb81d1e81ccbfb2", "start_char": 0, "end_char": 2342, "text_sha256": "2d6f134f9da5ac532fac9c58757e80a0b51c9912f8ddbec39eb81d1e81ccbfb2"} [ala-p24334290] Variant non ketotic hyperglycinemia is caused by mutations in LIAS, BOLA3 and the novel gene GLRX5. (2014). https://pubmed.ncbi.nlm.nih.gov/24334290/ DOI: 10.1093/brain/awt328
    Complete structured claim and evidence

  2. Isolated mouse embryonic mitochondria converted labeled glycine carbon into formate.

    Glycine → Formate source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Handoff to existing PLP-dependent glycine decarboxylase and lipoyl-GCSH/AMT folate transfer evidence; not new deficiency evidence.
    experimental_model
    Radiolabeled mitochondrial flux assay
    exposure
    Assay conditions described in the linked primary study.
    limitations
    No B6 or lipoate dietary perturbation tested.
    nutrient_topic
    Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)
    organism
    Mus musculus
    plain_language
    Glycine cleavage can feed folate-bound carbon into mitochondrial formate production.
    primary_references
    [pike-2010] Mitochondrial C1-tetrahydrofolate synthase (MTHFD1L) supports the flow of mitochondrial one-carbon units into the methyl cycle in embryos (2010). https://pubmed.ncbi.nlm.nih.gov/19948730/ DOI: 10.1074/jbc.m109.079855
    tissue_or_cell_type
    Embryonic mitochondria

    Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1096–1107

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiolabeled mitochondrial flux assay · source_derived_draft · unverified_draft

    ### embryonic-glycine-formate Isolated mouse embryonic mitochondria converted labeled glycine carbon into formate. Condition category: normal nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glycine cleavage can feed folate-bound carbon into mitochondrial formate production. organism: Mus musculus tissue_or_cell_type: Embryonic mitochondria experimental_model: Radiolabeled mitochondrial flux assay limitations: No B6 or lipoate dietary perturbation tested. exposure: Assay conditions described in the linked primary study. cross_nutrient: Handoff to existing PLP-dependent glycine decarboxylase and lipoyl-GCSH/AMT folate transfer evidence; not new deficiency evidence. [pike-2010] Mitochondrial C1-tetrahydrofolate synthase (MTHFD1L) supports the flow of mitochondrial one-carbon units into the methyl cycle in embryos (2010). https://pubmed.ncbi.nlm.nih.gov/19948730/ DOI: 10.1074/jbc.m109.079855
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards