Component

Mouse long-chain acyl-CoA dehydrogenase / Acadl

Mouse long-chain acyl-CoA dehydrogenase / Acadl

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 increased hepatic ACADL mRNA in the high-fat-fed mouse experiment.

    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 increased hepatic ACADL mRNA in the high-fat-fed mouse experiment.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
    experimental_model
    100 mg/kg intraperitoneally daily, 7 days.
    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 increased hepatic ACADL mRNA in the high-fat-fed mouse experiment.
    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-acadl; Transcript abundance is not enzyme activity or measured fatty-acid oxidation flux.

    Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 264–270

    AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 100 mg/kg intraperitoneally daily, 7 days. · Recorded from source · Recorded from source

    ### api-mouse-acadl Apigenin increased hepatic ACADL mRNA in the high-fat-fed mouse experiment. Transcript abundance is not enzyme activity or measured fatty-acid oxidation flux. Model and exposure: 100 mg/kg intraperitoneally daily, 7 days. 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.