Component

D-Glyceraldehyde 3-phosphate

Three-carbon sugar phosphate released in the transketolase donor half-reaction.

8 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.

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

Where it participates (unsigned role)

  1. Benfotiamine inhibited AGE-pathway activation in the experimental hyperglycemia models.

    Experimental context and source evidence
    experimental_model
    High-glucose bovine endothelial cells and diabetic rat retinal experiments.
    exposure
    Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
    limitations
    Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Bos taurus; Rattus norvegicus
    plain_language
    Less activation of a glycation pathway accompanied the intervention.
    primary_references
    [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    tissue_or_cell_type
    Endothelial cultures and retina

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1903–1913

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft

    ### b1-benfotiamine-age Benfotiamine inhibited AGE-pathway activation in the experimental hyperglycemia models. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less activation of a glycation pathway accompanied the intervention. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    Complete structured claim and evidence
  2. Benfotiamine inhibited hyperglycemia-associated hexosamine-pathway activation in the tested models.

    Benfotiamine → Hexosamine pathway activity source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    High-glucose bovine endothelial cells and diabetic rat retinal experiments.
    exposure
    Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
    limitations
    Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Bos taurus; Rattus norvegicus
    plain_language
    The intervention reduced one pathway fed by excess sugar intermediates.
    primary_references
    [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    tissue_or_cell_type
    Endothelial cultures and retina

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1891–1901

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft

    ### b1-benfotiamine-hexosamine Benfotiamine inhibited hyperglycemia-associated hexosamine-pathway activation in the tested models. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The intervention reduced one pathway fed by excess sugar intermediates. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    Complete structured claim and evidence
  3. Benfotiamine inhibited hyperglycemia-associated NF-kappaB activation in the tested models.

    Benfotiamine → NF-kappaB family source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    High-glucose bovine endothelial cells and diabetic rat retinal experiments.
    exposure
    Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
    limitations
    Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Bos taurus; Rattus norvegicus
    plain_language
    An inflammatory signaling readout also declined in these experiments.
    primary_references
    [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    tissue_or_cell_type
    Endothelial cultures and retina

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1927–1937

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft

    ### b1-benfotiamine-nfkb Benfotiamine inhibited hyperglycemia-associated NF-kappaB activation in the tested models. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inflammatory signaling readout also declined in these experiments. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    Complete structured claim and evidence
  4. Benfotiamine inhibited hyperglycemia-associated DAG-PKC pathway activation in the tested models.

    Benfotiamine → Protein kinase C family source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    High-glucose bovine endothelial cells and diabetic rat retinal experiments.
    exposure
    Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
    limitations
    Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Bos taurus; Rattus norvegicus
    plain_language
    Sugar processing was linked to a lipid-signaling pathway response.
    primary_references
    [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    tissue_or_cell_type
    Endothelial cultures and retina

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1915–1925

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft

    ### b1-benfotiamine-pkc Benfotiamine inhibited hyperglycemia-associated DAG-PKC pathway activation in the tested models. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sugar processing was linked to a lipid-signaling pathway response. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    Complete structured claim and evidence
  5. Benfotiamine prevented experimental diabetic retinopathy in the rat model reported by Hammes and colleagues.

    Benfotiamine → Diabetic retinal microvascular damage source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    High-glucose bovine endothelial cells and diabetic rat retinal experiments.
    exposure
    Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
    limitations
    Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Bos taurus; Rattus norvegicus
    plain_language
    The retinal disease endpoint improved in this animal experiment.
    primary_references
    [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    tissue_or_cell_type
    Endothelial cultures and retina

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1939–1949

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft

    ### b1-benfotiamine-rat-retinopathy Benfotiamine prevented experimental diabetic retinopathy in the rat model reported by Hammes and colleagues. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The retinal disease endpoint improved in this animal experiment. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    Complete structured claim and evidence
  6. Benfotiamine increased retinal transketolase activity in diabetic rats.

    Benfotiamine → Retinal transketolase activity source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    High-glucose bovine endothelial cells and diabetic rat retinal experiments.
    exposure
    Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
    limitations
    Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Bos taurus; Rattus norvegicus
    plain_language
    A B1 derivative increased a carbon-transfer enzyme activity in the diabetic retina.
    primary_references
    [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    tissue_or_cell_type
    Endothelial cultures and retina

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1879–1889

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft

    ### b1-benfotiamine-tkt Benfotiamine increased retinal transketolase activity in diabetic rats. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A B1 derivative increased a carbon-transfer enzyme activity in the diabetic retina. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
    Complete structured claim and evidence
  7. Acid-quench NMR of human TKT identified the protonated form of the DHE-ThDP intermediate generated during the donor half-reaction.

    Experimental context and source evidence
    evidence
    [{"paper_key": "mitschke-2010-tkt", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-31", "p-44", "p-46", "p-47"], "locator": "acid quench", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}]
    experimental_model
    Human recombinant TKT; chemical quench and NMR.
    limitations
    Acid quench protonates the intermediate; native enamine occupancy is inferred from trapped species.
    nutrient
    Thiamine (vitamin B1) · Thiamine (vitamin B1)
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Homo sapiens
    plain_language
    B1 temporarily carries the two-carbon sugar fragment before its transfer to an acceptor; the detected acid-trapped form is distinguished from the reactive enamine.
    primary_references
    [mitschke-2010-tkt] The crystal structure of human transketolase and new insights into its mode of action (2010). https://pubmed.ncbi.nlm.nih.gov/20667822/ DOI: 10.1074/jbc.m110.149955
    tissue_or_cell_type
    Purified enzyme

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 963–974

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human recombinant TKT; chemical quench and NMR. · source_derived_draft · unverified_draft

    ### b1-tkt-dhe-thdp-intermediate Acid-quench NMR of human TKT identified the protonated form of the DHE-ThDP intermediate generated during the donor half-reaction. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: B1 temporarily carries the two-carbon sugar fragment before its transfer to an acceptor; the detected acid-trapped form is distinguished from the reactive enamine. organism: Homo sapiens tissue_or_cell_type: Purified enzyme experimental_model: Human recombinant TKT; chemical quench and NMR. limitations: Acid quench protonates the intermediate; native enamine occupancy is inferred from trapped species. evidence: [{"paper_key": "mitschke-2010-tkt", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-31", "p-44", "p-46", "p-47"], "locator": "acid quench", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}] nutrient: Thiamine (vitamin B1) [mitschke-2010-tkt] The crystal structure of human transketolase and new insights into its mode of action (2010). https://pubmed.ncbi.nlm.nih.gov/20667822/ DOI: 10.1074/jbc.m110.149955
    Complete structured claim and evidence
  8. Human TKT transfers two carbons from xylulose-5-phosphate to ribose-5-phosphate, yielding glyceraldehyde-3-phosphate and sedoheptulose-7-phosphate.

    Experimental context and source evidence
    evidence
    [{"paper_key": "mitschke-2010-tkt", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-12"], "locator": "simplified reaction scheme", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}]
    experimental_model
    Recombinant human TKT reaction analysis.
    limitations
    Direct reaction chemistry; indirect recycling effects on oxidative PPP flux need separate evidence.
    nutrient
    Thiamine (vitamin B1) · Thiamine (vitamin B1)
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Homo sapiens
    plain_language
    B1 supports sugar rearrangement, connecting pentose and glycolytic intermediates. This reaction does not directly make NADPH.
    primary_references
    [mitschke-2010-tkt] The crystal structure of human transketolase and new insights into its mode of action (2010). https://pubmed.ncbi.nlm.nih.gov/20667822/ DOI: 10.1074/jbc.m110.149955
    tissue_or_cell_type
    Purified enzyme

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 950–961

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human TKT reaction analysis. · source_derived_draft · unverified_draft

    ### b1-tkt-nonoxidative-carbon-transfer Human TKT transfers two carbons from xylulose-5-phosphate to ribose-5-phosphate, yielding glyceraldehyde-3-phosphate and sedoheptulose-7-phosphate. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: B1 supports sugar rearrangement, connecting pentose and glycolytic intermediates. This reaction does not directly make NADPH. organism: Homo sapiens tissue_or_cell_type: Purified enzyme experimental_model: Recombinant human TKT reaction analysis. limitations: Direct reaction chemistry; indirect recycling effects on oxidative PPP flux need separate evidence. evidence: [{"paper_key": "mitschke-2010-tkt", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-12"], "locator": "simplified reaction scheme", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}] nutrient: Thiamine (vitamin B1) [mitschke-2010-tkt] The crystal structure of human transketolase and new insights into its mode of action (2010). https://pubmed.ncbi.nlm.nih.gov/20667822/ DOI: 10.1074/jbc.m110.149955
    Complete structured claim and evidence

In the sources

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

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