Component

Mouse peroxisome proliferator-activated receptor alpha / Ppara

Context-specific entity; species, compartment and exposure are stated on each claim.

3 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 it acts on

  1. PPARalpha directly induced hepatic FGF21 in response to fasting or agonists.

    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse fasting, agonist and FGF21 experiments.
    limitations
    Species-specific experimental evidence; not a human fasting timer.
    nutrient_topic
    Fasting physiological-state collection; human protocols, cellular deprivation and refeeding are distinguished. · Fasting / abstention from energy intake
    plain_language
    A fat-sensing regulator activated an endocrine signal.
    primary_references
    Endocrine regulation of the fasting response by PPARalpha-mediated induction of fibroblast growth factor 21. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17550777/ · DOI 10.1016/j.cmet.2007.05.003

    Fasting: fuel switching, nutrient sensing, ketone signaling, nutrient dependencies and refeeding (2026-09-18) · lines 240–246

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse fasting, agonist and FGF21 experiments. · source_derived_draft · unverified_draft

    ## fast-mouse-fgf A fat-sensing regulator activated an endocrine signal. PPARalpha directly induced hepatic FGF21 in response to fasting or agonists. Model: Mouse fasting, agonist and FGF21 experiments. Limitations: Species-specific experimental evidence; not a human fasting timer. Evidence access: Primary abstract Endocrine regulation of the fasting response by PPARalpha-mediated induction of fibroblast growth factor 21. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17550777/ · DOI 10.1016/j.cmet.2007.05.003
    Complete structured claim and evidence

What acts on it

  1. Ankaflavin increased hepatic PPAR-alpha expression and promoted a fatty-acid-oxidation program in the mouse study.

    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    High-fat-diet C57BL/6 mice; related mouse FL83B hepatocyte experiments also reported.
    limitations
    The paper describes agonist activity; the accessed abstract does not resolve direct receptor affinity or establish a human clinical effect.
    nutrient_topic
    Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
    plain_language
    A transcriptional program provides a distinct route from statin inhibition.
    primary_references
    [24275089] Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24275089/ · DOI 10.1016/j.fct.2013.11.015

    Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 228–234

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · High-fat-diet C57BL/6 mice; related mouse FL83B hepatocyte experiments also reported. · source_derived_draft · unverified_draft

    ## red-yeast-rice-ankaflavin-ppara A transcriptional program provides a distinct route from statin inhibition. Ankaflavin increased hepatic PPAR-alpha expression and promoted a fatty-acid-oxidation program in the mouse study. Model: High-fat-diet C57BL/6 mice; related mouse FL83B hepatocyte experiments also reported. Limitations: The paper describes agonist activity; the accessed abstract does not resolve direct receptor affinity or establish a human clinical effect. Evidence access: Primary abstract [24275089] Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24275089/ · DOI 10.1016/j.fct.2013.11.015
    Complete structured claim and evidence
  2. Monascin increased hepatic PPAR-alpha expression and promoted a fatty-acid-oxidation program in the mouse study.

    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    High-fat-diet C57BL/6 mice; related mouse FL83B hepatocyte experiments also reported.
    limitations
    The paper describes agonist activity; the accessed abstract does not resolve direct receptor affinity or establish a human clinical effect.
    nutrient_topic
    Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
    plain_language
    A transcriptional program provides a distinct route from statin inhibition.
    primary_references
    [24275089] Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24275089/ · DOI 10.1016/j.fct.2013.11.015

    Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 212–218

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · High-fat-diet C57BL/6 mice; related mouse FL83B hepatocyte experiments also reported. · source_derived_draft · unverified_draft

    ## red-yeast-rice-monascin-ppara A transcriptional program provides a distinct route from statin inhibition. Monascin increased hepatic PPAR-alpha expression and promoted a fatty-acid-oxidation program in the mouse study. Model: High-fat-diet C57BL/6 mice; related mouse FL83B hepatocyte experiments also reported. Limitations: The paper describes agonist activity; the accessed abstract does not resolve direct receptor affinity or establish a human clinical effect. Evidence access: Primary abstract [24275089] Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24275089/ · DOI 10.1016/j.fct.2013.11.015
    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