Component

Mouse dihydrolipoamide dehydrogenase / Dld

Mus musculus DLD component of mitochondrial ketoacid dehydrogenases and glycine cleavage system.

3 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. DLD activity in Slc25a32-null embryo mitochondria was about 23.9% of wild-type control.

    Slc25a32-null mouse genotype → Mouse dihydrolipoamide dehydrogenase / Dld source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    DLD links B2 cofactor supply to glycine cleavage and thus folate-mediated one-carbon metabolism.
    evidence_spans
    [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 43, "char_start": 0, "char_end": 1215, "evidence_access": "full-text"}]
    experimental_model
    Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays.
    exposure
    Slc25a32-null versus wild-type embryos.
    limitations
    Knockout affects multiple flavoproteins; DLD-specific genetic rescue was not performed.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Mus musculus
    plain_language
    A defect in mitochondrial flavin supply impaired the shared DLD enzyme.
    primary_references
    [peng-2022-slc25a32] Mitochondrial FAD shortage in SLC25A32 deficiency affects folate-mediated one-carbon metabolism (2022). https://pubmed.ncbi.nlm.nih.gov/35727412/ DOI: 10.1007/s00018-022-04404-0
    tissue_or_cell_type
    Embryo mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 874–886

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays. · source_derived_draft · unverified_draft

    ### b2-met-mouse-null-dld-activity DLD activity in Slc25a32-null embryo mitochondria was about 23.9% of wild-type control. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A defect in mitochondrial flavin supply impaired the shared DLD enzyme. organism: Mus musculus tissue_or_cell_type: Embryo mitochondria experimental_model: Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays. limitations: Knockout affects multiple flavoproteins; DLD-specific genetic rescue was not performed. exposure: Slc25a32-null versus wild-type embryos. cross_nutrient: DLD links B2 cofactor supply to glycine cleavage and thus folate-mediated one-carbon metabolism. evidence_spans: [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 43, "char_start": 0, "char_end": 1215, "evidence_access": "full-text"}] [peng-2022-slc25a32] Mitochondrial FAD shortage in SLC25A32 deficiency affects folate-mediated one-carbon metabolism (2022). https://pubmed.ncbi.nlm.nih.gov/35727412/ DOI: 10.1007/s00018-022-04404-0
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Maternal sodium formate supplementation increased embryo CH3-THF in Slc25a32-null offspring that completed neural tube closure.

    Formate → 5-Methyltetrahydrofolate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Demonstrates a formate-to-folate consequence downstream of a mitochondrial flavin-supply defect, not dietary folate deficiency.
    evidence_spans
    [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 38, "char_start": 0, "char_end": 1062, "evidence_access": "full-text"}]
    experimental_model
    Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays.
    exposure
    Dams received 0.1 mol/L sodium formate in drinking water; experimental context only.
    limitations
    Analyzed responder subgroup; does not prove normal folate metabolism or bypass every effect of Slc25a32 loss.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Mus musculus
    plain_language
    Supplying a missing one-carbon donor changed the downstream folate profile.
    primary_references
    [peng-2022-slc25a32] Mitochondrial FAD shortage in SLC25A32 deficiency affects folate-mediated one-carbon metabolism (2022). https://pubmed.ncbi.nlm.nih.gov/35727412/ DOI: 10.1007/s00018-022-04404-0
    tissue_or_cell_type
    Whole E11.5 embryos
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 902–914

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays. · source_derived_draft · unverified_draft

    ### b2-met-formate-embryo-folate-rescue Maternal sodium formate supplementation increased embryo CH3-THF in Slc25a32-null offspring that completed neural tube closure. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Supplying a missing one-carbon donor changed the downstream folate profile. organism: Mus musculus tissue_or_cell_type: Whole E11.5 embryos experimental_model: Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays. limitations: Analyzed responder subgroup; does not prove normal folate metabolism or bypass every effect of Slc25a32 loss. exposure: Dams received 0.1 mol/L sodium formate in drinking water; experimental context only. cross_nutrient: Demonstrates a formate-to-folate consequence downstream of a mitochondrial flavin-supply defect, not dietary folate deficiency. evidence_spans: [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 38, "char_start": 0, "char_end": 1062, "evidence_access": "full-text"}] [peng-2022-slc25a32] Mitochondrial FAD shortage in SLC25A32 deficiency affects folate-mediated one-carbon metabolism (2022). https://pubmed.ncbi.nlm.nih.gov/35727412/ DOI: 10.1007/s00018-022-04404-0
    Complete structured claim and evidence

  2. Isolated Slc25a32-null embryo mitochondria produced about 10.6% of control labeled formate from [13C2]-glycine over 24 hours.

    Slc25a32-null mouse genotype → Mitochondrial glycine-derived formate production source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    B2-dependent mitochondrial function supports glycine carbon entry into folate-related one-carbon supply.
    evidence_spans
    [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 43, "char_start": 0, "char_end": 1215, "evidence_access": "full-text"}]
    experimental_model
    Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays.
    exposure
    Slc25a32-null mitochondria supplied [1,2-13C2]-glycine.
    limitations
    Long isolated-mitochondrial assay; this is glycine-derived flux, not total cellular formate synthesis.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Mus musculus
    plain_language
    The same genetic defect sharply reduced one-carbon output from glycine.
    primary_references
    [peng-2022-slc25a32] Mitochondrial FAD shortage in SLC25A32 deficiency affects folate-mediated one-carbon metabolism (2022). https://pubmed.ncbi.nlm.nih.gov/35727412/ DOI: 10.1007/s00018-022-04404-0
    tissue_or_cell_type
    Embryo mitochondria, 24-hour isotope incubation
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 888–900

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays. · source_derived_draft · unverified_draft

    ### b2-met-mouse-null-glycine-formate Isolated Slc25a32-null embryo mitochondria produced about 10.6% of control labeled formate from [13C2]-glycine over 24 hours. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same genetic defect sharply reduced one-carbon output from glycine. organism: Mus musculus tissue_or_cell_type: Embryo mitochondria, 24-hour isotope incubation experimental_model: Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays. limitations: Long isolated-mitochondrial assay; this is glycine-derived flux, not total cellular formate synthesis. exposure: Slc25a32-null mitochondria supplied [1,2-13C2]-glycine. cross_nutrient: B2-dependent mitochondrial function supports glycine carbon entry into folate-related one-carbon supply. evidence_spans: [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 43, "char_start": 0, "char_end": 1215, "evidence_access": "full-text"}] [peng-2022-slc25a32] Mitochondrial FAD shortage in SLC25A32 deficiency affects folate-mediated one-carbon metabolism (2022). https://pubmed.ncbi.nlm.nih.gov/35727412/ DOI: 10.1007/s00018-022-04404-0
    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