Human free fatty acid receptor 3 / FFAR3

evidence_span

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experimental_model

Ligand bank screening in yeast, confirmed by calcium mobilisation, GTP-gamma-S binding and oocyte coexpression

exposure

Short chain carboxylic acid anions applied to recombinant GPR41 and GPR43

limitations

The deorphanising paper. Potencies come from recombinant systems, not from tissue, and the authors state plainly that the cognate physiological ligands are not clear.

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

Human and mouse receptors

plain_language

A sister receptor prefers longer fatty acids, and the two sit in different tissues.

primary_references

[acetate-p12496283] The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acids. (2003). https://pubmed.ncbi.nlm.nih.gov/12496283/ DOI: 10.1074/jbc.m211609200

tissue_or_cell_type

Transfected mammalian cells and Xenopus oocytes

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 238–249

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ligand bank screening in yeast, confirmed by calcium mobilisation, GTP-gamma-S binding and oocyte coexpression · source_derived_draft · unverified_draft

### acetate-ffar3-chain-length GPR41 is 52% similar and 43% identical to GPR43 and was activated by similar ligands but with differing specificity for carbon chain length, pentanoate being its most potent agonist; GPR41 was expressed primarily in adipose tissue while the highest levels of GPR43 were in immune cells, and a third family member GPR42 is most likely a recent gene duplication of GPR41 and may be a pseudogene. 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: A sister receptor prefers longer fatty acids, and the two sit in different tissues. organism: Human and mouse receptors tissue_or_cell_type: Transfected mammalian cells and Xenopus oocytes experimental_model: Ligand bank screening in yeast, confirmed by calcium mobilisation, GTP-gamma-S binding and oocyte coexpression limitations: The deorphanising paper. Potencies come from recombinant systems, not from tissue, and the authors state plainly that the cognate physiological ligands are not clear. exposure: Short chain carboxylic acid anions applied to recombinant GPR41 and GPR43 evidence_span: {"source_cache": "artifacts/acetate-research/12496283.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "83f7777cab02a7c69f063d21e26f895884724f46ad539ebc767d9e6f371bf64f", "start_char": 0, "end_char": 1291, "text_sha256": "83f7777cab02a7c69f063d21e26f895884724f46ad539ebc767d9e6f371bf64f"} [acetate-p12496283] The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acids. (2003). https://pubmed.ncbi.nlm.nih.gov/12496283/ DOI: 10.1074/jbc.m211609200

evidence_span

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experimental_model

Transgenic monomeric red fluorescent protein reporter mice with FACS purification and quantitative PCR

exposure

Cell-type resolved expression of FFAR2 and FFAR3 reporters, with receptor-specific synthetic agonists on colonic crypt cultures

limitations

Reporter expression is not the same as receptor protein. The FFAR2 result here is weaker in enteroendocrine cells than the rat immunohistochemistry in this collection reports.

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 FFAR3 reporter marks nearly every hormone-making cell of the gut, and the gut nerves as well.

primary_references

[acetate-p23885020] GPR41/FFAR3 and GPR43/FFAR2 as cosensors for short-chain fatty acids in enteroendocrine cells vs FFAR3 in enteric neurons and FFAR2 in enteric leukocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/23885020/ DOI: 10.1210/en.2013-1142

tissue_or_cell_type

Whole gastrointestinal tract

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 290–301

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transgenic monomeric red fluorescent protein reporter mice with FACS purification and quantitative PCR · source_derived_draft · unverified_draft

### acetate-ffar3-on-l-cells The FFAR3 reporter was strongly expressed in all cholecystokinin, glucose-dependent insulinotropic peptide and secretin cells of the proximal small intestine, in all GLP-1, peptide YY and neurotensin cells of the distal small intestine, and in the large population of peptide YY and GLP-1 cells throughout the colon and rectum, and also in the neuronal cells of the submucosal and myenteric ganglia. 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 FFAR3 reporter marks nearly every hormone-making cell of the gut, and the gut nerves as well. organism: Mouse tissue_or_cell_type: Whole gastrointestinal tract experimental_model: Transgenic monomeric red fluorescent protein reporter mice with FACS purification and quantitative PCR limitations: Reporter expression is not the same as receptor protein. The FFAR2 result here is weaker in enteroendocrine cells than the rat immunohistochemistry in this collection reports. exposure: Cell-type resolved expression of FFAR2 and FFAR3 reporters, with receptor-specific synthetic agonists on colonic crypt cultures evidence_span: {"source_cache": "artifacts/acetate-research/23885020.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b834455e11c2b8fa3c4c19c5d01375815e46c3b0f8e25eb184f0eaa6a51c749e", "start_char": 0, "end_char": 2144, "text_sha256": "b834455e11c2b8fa3c4c19c5d01375815e46c3b0f8e25eb184f0eaa6a51c749e"} [acetate-p23885020] GPR41/FFAR3 and GPR43/FFAR2 as cosensors for short-chain fatty acids in enteroendocrine cells vs FFAR3 in enteric neurons and FFAR2 in enteric leukocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/23885020/ DOI: 10.1210/en.2013-1142

evidence_access

Primary abstract

experimental_model

Human recombinant receptor signaling assays.

limitations

FFAR3 and FFAR2 are separate proteins, not alternative names for one receptor.

nutrient_topic

Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate

plain_language

A second receptor recognized overlapping molecules with different preferences.

primary_references

The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acids. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12496283/ · DOI 10.1074/jbc.M211609200

Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 510–516

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant receptor signaling assays. · source_derived_draft · unverified_draft

## butyrate-ffar3-agonist A second receptor recognized overlapping molecules with different preferences. Butyrate was an agonist at human GPR41/FFAR3, whose chain-length preference differed from GPR43. Model: Human recombinant receptor signaling assays. Limitations: FFAR3 and FFAR2 are separate proteins, not alternative names for one receptor. Evidence access: Primary abstract The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acids. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12496283/ · DOI 10.1074/jbc.M211609200

evidence_span

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experimental_model

Isolated perfused rat colon with luminal and vascular short-chain fatty acid infusion and receptor pharmacology

exposure

Acetate, propionate and butyrate perfused luminally or vascularly, with FFAR2/FFAR3 agonists, an FFAR3 antagonist, nifedipine, diazoxide and 2,4-dinitrophenol

limitations

An isolated organ preparation with an intact blood supply. It reaches the opposite mechanistic conclusion from the knockout work in this collection and is why the receptor route is recorded as disputed.

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

Rat

plain_language

Blocking the receptors changed nothing, while blocking energy production abolished the response.

primary_references

[acetate-p29494208] The impact of short-chain fatty acids on GLP-1 and PYY secretion from the isolated perfused rat colon. (2018). https://pubmed.ncbi.nlm.nih.gov/29494208/ DOI: 10.1152/ajpgi.00346.2017

tissue_or_cell_type

Colon

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 342–353

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated perfused rat colon with luminal and vascular short-chain fatty acid infusion and receptor pharmacology · source_derived_draft · unverified_draft

### acetate-receptor-not-required A FFAR2- and FFAR3-specific agonist had no effect on colonic GLP-1 output and a FFAR3 antagonist did not decrease the short-chain fatty acid-induced GLP-1 response, whereas the calcium channel blocker nifedipine, the KATP-channel opener diazoxide and the ATP synthesis inhibitor 2,4-dinitrophenol completely abolished the responses, leading the authors to conclude that the fatty acids are metabolised and function as a colonocyte energy source rather than acting through the receptors. 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: Blocking the receptors changed nothing, while blocking energy production abolished the response. organism: Rat tissue_or_cell_type: Colon experimental_model: Isolated perfused rat colon with luminal and vascular short-chain fatty acid infusion and receptor pharmacology limitations: An isolated organ preparation with an intact blood supply. It reaches the opposite mechanistic conclusion from the knockout work in this collection and is why the receptor route is recorded as disputed. exposure: Acetate, propionate and butyrate perfused luminally or vascularly, with FFAR2/FFAR3 agonists, an FFAR3 antagonist, nifedipine, diazoxide and 2,4-dinitrophenol evidence_span: {"source_cache": "artifacts/acetate-research/29494208.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9f8def7b832fdd5d5aed67891c84b18b597d558d9361a92412ccc44264b88126", "start_char": 0, "end_char": 2445, "text_sha256": "9f8def7b832fdd5d5aed67891c84b18b597d558d9361a92412ccc44264b88126"} [acetate-p29494208] The impact of short-chain fatty acids on GLP-1 and PYY secretion from the isolated perfused rat colon. (2018). https://pubmed.ncbi.nlm.nih.gov/29494208/ DOI: 10.1152/ajpgi.00346.2017