Component
Mouse free fatty acid receptor 3 / Ffar3
Context-specific entity; species, compartment and exposure are stated on each claim.
2 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
Ffar3-deficient mice retained the body-weight and food-intake effects of butyrate; FFAR3 had only a minor role in the GLP-1 response and was unnecessary for GIP induction.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse Ffar3 knockout intervention.
- limitations
- A receptor being activated does not make it necessary for every organism-level response.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- Removing one receptor left much of the response intact.
- primary_references
- Butyrate and propionate protect against diet-induced obesity and regulate gut hormones via free fatty acid receptor 3-independent mechanisms. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22506074/ · DOI 10.1371/journal.pone.0035240
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 542–548
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse Ffar3 knockout intervention. · source_derived_draft · unverified_draft
## butyrate-ffar3-loss-residual Removing one receptor left much of the response intact. Ffar3-deficient mice retained the body-weight and food-intake effects of butyrate; FFAR3 had only a minor role in the GLP-1 response and was unnecessary for GIP induction. Model: Mouse Ffar3 knockout intervention. Limitations: A receptor being activated does not make it necessary for every organism-level response. Evidence access: Primary abstract Butyrate and propionate protect against diet-induced obesity and regulate gut hormones via free fatty acid receptor 3-independent mechanisms. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22506074/ · DOI 10.1371/journal.pone.0035240
Complete structured claim and evidence
Where it participates (unsigned role)
Butyrate administration induced GLP-1/GIP responses and reduced food intake in the mouse study.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse dietary and acute SCFA experiments.
- limitations
- Not a human appetite or weight-loss trial.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- Gut hormone release accompanied reduced feeding.
- primary_references
- Butyrate and propionate protect against diet-induced obesity and regulate gut hormones via free fatty acid receptor 3-independent mechanisms. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22506074/ · DOI 10.1371/journal.pone.0035240
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 534–540
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse dietary and acute SCFA experiments. · source_derived_draft · unverified_draft
## butyrate-gut-hormones Gut hormone release accompanied reduced feeding. Butyrate administration induced GLP-1/GIP responses and reduced food intake in the mouse study. Model: Mouse dietary and acute SCFA experiments. Limitations: Not a human appetite or weight-loss trial. Evidence access: Primary abstract Butyrate and propionate protect against diet-induced obesity and regulate gut hormones via free fatty acid receptor 3-independent mechanisms. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22506074/ · DOI 10.1371/journal.pone.0035240
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.