Component
Insulin signalling in adipocytes
Insulin signalling in adipocytes. Species, exposure and limitations are retained in each linked claim.
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.
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 acts on it
Short-chain fatty acid-mediated activation of GPR43 suppressed insulin signalling in adipocytes, which inhibited fat accumulation in adipose tissue and promoted the metabolism of unincorporated lipids and glucose in other tissues, establishing GPR43 as a sensor for excessive dietary energy.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/acetate-research/23652017.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "52bcd2cce838e217b7115f23092863912a2fad5dbece809485fa06c9c06d8d60", "start_char": 0, "end_char": 1122, "text_sha256": "52bcd2cce838e217b7115f23092863912a2fad5dbece809485fa06c9c06d8d60"}
- experimental_model
- GPR43-deficient and adipose-overexpressing mice, raised conventionally, germ-free and after antibiotics
- exposure
- Normal and high-fat diet, with germ-free rearing and antibiotic treatment as controls
- limitations
- The germ-free control is what ties the receptor phenotype to microbial short-chain fatty acids rather than to the receptor alone. The receptor senses all short-chain fatty acids, not acetate specifically.
- nutrient_topic
- Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
- organism
- Mouse
- plain_language
- The signal tells fat cells to stop taking on more, and sends the fuel elsewhere.
- primary_references
- [acetate-p23652017] The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43. (2013). https://pubmed.ncbi.nlm.nih.gov/23652017/ DOI: 10.1038/ncomms2852
- tissue_or_cell_type
- Adipose tissue and whole body
Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 264–275
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GPR43-deficient and adipose-overexpressing mice, raised conventionally, germ-free and after antibiotics · source_derived_draft · unverified_draft
### acetate-ffar2-insulin-signalling Short-chain fatty acid-mediated activation of GPR43 suppressed insulin signalling in adipocytes, which inhibited fat accumulation in adipose tissue and promoted the metabolism of unincorporated lipids and glucose in other tissues, establishing GPR43 as a sensor for excessive dietary energy. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: The signal tells fat cells to stop taking on more, and sends the fuel elsewhere. organism: Mouse tissue_or_cell_type: Adipose tissue and whole body experimental_model: GPR43-deficient and adipose-overexpressing mice, raised conventionally, germ-free and after antibiotics limitations: The germ-free control is what ties the receptor phenotype to microbial short-chain fatty acids rather than to the receptor alone. The receptor senses all short-chain fatty acids, not acetate specifically. exposure: Normal and high-fat diet, with germ-free rearing and antibiotic treatment as controls evidence_span: {"source_cache": "artifacts/acetate-research/23652017.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "52bcd2cce838e217b7115f23092863912a2fad5dbece809485fa06c9c06d8d60", "start_char": 0, "end_char": 1122, "text_sha256": "52bcd2cce838e217b7115f23092863912a2fad5dbece809485fa06c9c06d8d60"} [acetate-p23652017] The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43. (2013). https://pubmed.ncbi.nlm.nih.gov/23652017/ DOI: 10.1038/ncomms2852
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.