Component

D-Xylulose 5-phosphate

Ketose-phosphate donor in the nonoxidative pentose phosphate pathway.

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

Where it participates (unsigned role)

  1. Acid-quench NMR of human TKT identified the protonated form of the DHE-ThDP intermediate generated during the donor half-reaction.

    Human transketolase → 1,2-Dihydroxyethyl-ThDP intermediate source_derived_draftungraded
    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

  2. Human TKT transfers two carbons from xylulose-5-phosphate to ribose-5-phosphate, yielding glyceraldehyde-3-phosphate and sedoheptulose-7-phosphate.

    Human transketolase → Nonoxidative pentose phosphate pathway source_derived_draftungraded
    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

  3. In liver the concentration of xylulose-5-phosphate was significantly higher in the control group than in the acetic acid groups, and in gastrocnemius muscle the ratio of fructose-1,6-bisphosphate to fructose-6-phosphate was significantly higher in the control group; the authors proposed that acetic acid may activate gluconeogenesis and inactivate glycolysis in liver through suppression of xylulose-5-phosphate accumulation, and inhibit glycolysis in skeletal muscle by suppressing phosphofructokinase-1 activity.

    Acetic acid → Glycolysis source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/acetate-research/11435516.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e", "start_char": 0, "end_char": 1638, "text_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e"}
    experimental_model
    Food-deprived rats given graded dietary acetic acid for 2 hours
    exposure
    0, 0.1, 0.2 or 0.4 g acetic acid per 100 g diet for 2 hours after 15 hours of food deprivation
    limitations
    Only the 0.2 g dose reached significance for glycogen, so the dose-response is not monotonic. The glycolytic mechanism is the authors’ inference from metabolite ratios, not a direct enzyme measurement.
    nutrient_topic
    Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
    organism
    Rat
    plain_language
    The acid appears to slow the burning of glucose, which is why more of it ends up stored.
    primary_references
    [acetate-p11435516] Acetic acid feeding enhances glycogen repletion in liver and skeletal muscle of rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11435516/ DOI: 10.1093/jn/131.7.1973
    tissue_or_cell_type
    Liver and skeletal muscle

    Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 446–457

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Food-deprived rats given graded dietary acetic acid for 2 hours · source_derived_draft · unverified_draft

    ### acetate-acetate-inhibits-glycolysis In liver the concentration of xylulose-5-phosphate was significantly higher in the control group than in the acetic acid groups, and in gastrocnemius muscle the ratio of fructose-1,6-bisphosphate to fructose-6-phosphate was significantly higher in the control group; the authors proposed that acetic acid may activate gluconeogenesis and inactivate glycolysis in liver through suppression of xylulose-5-phosphate accumulation, and inhibit glycolysis in skeletal muscle by suppressing phosphofructokinase-1 activity. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: The acid appears to slow the burning of glucose, which is why more of it ends up stored. organism: Rat tissue_or_cell_type: Liver and skeletal muscle experimental_model: Food-deprived rats given graded dietary acetic acid for 2 hours limitations: Only the 0.2 g dose reached significance for glycogen, so the dose-response is not monotonic. The glycolytic mechanism is the authors’ inference from metabolite ratios, not a direct enzyme measurement. exposure: 0, 0.1, 0.2 or 0.4 g acetic acid per 100 g diet for 2 hours after 15 hours of food deprivation evidence_span: {"source_cache": "artifacts/acetate-research/11435516.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e", "start_char": 0, "end_char": 1638, "text_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e"} [acetate-p11435516] Acetic acid feeding enhances glycogen repletion in liver and skeletal muscle of rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11435516/ DOI: 10.1093/jn/131.7.1973
    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