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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
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
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 evidenceMonascin 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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.