Component

Mouse glucose tolerance in the 2013 apigenin study

Mouse glucose tolerance in the 2013 apigenin study

1 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

What acts on it

  1. Apigenin improved glucose-tolerance readouts and lowered fasting glucose in high-fat-fed mice.

    Experimental context and source evidence
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_contrast
    {"intervention": "Apigenin", "comparator": "Vehicle", "endpoint": "Apigenin improved glucose-tolerance readouts and lowered fasting glucose in high-fat-fed mice.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
    experimental_model
    Same seven-day injection regimen.
    interpretation_status
    Recorded from source with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
    plain_language
    Apigenin improved glucose-tolerance readouts and lowered fasting glucose in high-fat-fed mice.
    primary_references
    Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
    source_locator
    Reviewed reference api-mouse-glucose; No clinical diabetes efficacy follows from this experiment.

    Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 272–278

    AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Same seven-day injection regimen. · Recorded from source · Recorded from source

    ### api-mouse-glucose Apigenin improved glucose-tolerance readouts and lowered fasting glucose in high-fat-fed mice. No clinical diabetes efficacy follows from this experiment. Model and exposure: Same seven-day injection regimen. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    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.