Human free fatty acid receptor 2 / FFAR2

evidence_span

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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

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

FFAR2 turned out to sit mainly on immune cells rather than on the hormone cells, though its agonist still released the hormone.

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 303–314

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-ffar2-mostly-leukocytes The FFAR2 reporter was strongly expressed in a large population of leukocytes in the lamina propria, particularly of the small intestine, but surprisingly only weakly in a subpopulation of enteroendocrine cells; nevertheless synthetic ligands specific for either FFAR3 or FFAR2 each released GLP-1 from colonic crypt cultures. 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: FFAR2 turned out to sit mainly on immune cells rather than on the hormone cells, though its agonist still released the hormone. 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_span

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experimental_model

RT-PCR, Western blotting and immunohistochemistry with a rat-specific GPR43 antiserum

exposure

Receptor localisation across mucosal cell types

limitations

An anatomical result naming the cells that carry the receptor. Localisation is not function, and the antiserum was raised against a synthesised fragment.

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

The receptor sits on the gut cells that make PYY, and on mast cells, but not on the serotonin-making gut cells.

primary_references

[acetate-p16453106] Short-chain fatty acid receptor, GPR43, is expressed by enteroendocrine cells and mucosal mast cells in rat intestine. (2006). https://pubmed.ncbi.nlm.nih.gov/16453106/ DOI: 10.1007/s00441-005-0140-x

tissue_or_cell_type

Distal ileum and 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 277–288

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · RT-PCR, Western blotting and immunohistochemistry with a rat-specific GPR43 antiserum · source_derived_draft · unverified_draft

### acetate-ffar2-on-pyy-cells GPR43 immunoreactivity was localised to enteroendocrine cells expressing peptide YY, whereas 5-hydroxytryptamine-immunoreactive enteroendocrine cells were not immunoreactive for GPR43, and mast cells of the lamina propria expressing 5-hydroxytryptamine were also GPR43-immunoreactive. 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 receptor sits on the gut cells that make PYY, and on mast cells, but not on the serotonin-making gut cells. organism: Rat tissue_or_cell_type: Distal ileum and colon experimental_model: RT-PCR, Western blotting and immunohistochemistry with a rat-specific GPR43 antiserum limitations: An anatomical result naming the cells that carry the receptor. Localisation is not function, and the antiserum was raised against a synthesised fragment. exposure: Receptor localisation across mucosal cell types evidence_span: {"source_cache": "artifacts/acetate-research/16453106.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14165574bceda6c6197de30baae79895b87d2b95272ea42c231554d7a4c015d2", "start_char": 0, "end_char": 1605, "text_sha256": "14165574bceda6c6197de30baae79895b87d2b95272ea42c231554d7a4c015d2"} [acetate-p16453106] Short-chain fatty acid receptor, GPR43, is expressed by enteroendocrine cells and mucosal mast cells in rat intestine. (2006). https://pubmed.ncbi.nlm.nih.gov/16453106/ DOI: 10.1007/s00441-005-0140-x

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

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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 receptor keeps fat off, and only when gut bacteria are there to supply its signal.

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

trigger_kind

machinery_impairment Imported condition classification; unverified.

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 251–262

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-suppresses-fat GPR43-deficient mice were obese on a normal diet whereas mice overexpressing GPR43 specifically in adipose tissue remained lean even when fed a high-fat diet, and raised under germ-free conditions or after treatment with antibiotics both types of mice had a normal phenotype. Condition category: machinery_impairment 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 receptor keeps fat off, and only when gut bacteria are there to supply its signal. 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

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

evidence_span

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experimental_model

Wistar rats, C57BL6 mice and FFA2 knockout mice, with colonic crypt cultures and portal vein sampling

exposure

Propionate applied to colonic crypt cultures and infused into the colon, with FFA2 deletion as the test of mediation

limitations

Establishes the receptor-to-hormone step in rodents using propionate rather than acetate. The knockout is the strength of the design.

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 and mouse

plain_language

In rodents the receptor is what releases the two gut hormones; delete it and the response goes.

primary_references

[acetate-p25109781] The short chain fatty acid propionate stimulates GLP-1 and PYY secretion via free fatty acid receptor 2 in rodents. (2015). https://pubmed.ncbi.nlm.nih.gov/25109781/ DOI: 10.1038/ijo.2014.153

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 316–327

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Wistar rats, C57BL6 mice and FFA2 knockout mice, with colonic crypt cultures and portal vein sampling · source_derived_draft · unverified_draft

### acetate-scfa-glp1-rodent Propionate stimulated secretion of both peptide YY and GLP-1 from wild-type murine colonic crypt cultures and this effect was significantly attenuated in cultures from FFA2 knockout mice, while intra-colonic infusion of propionate elevated both hormones in portal vein plasma in rats and mice but did not significantly stimulate their release in FFA2 knockout mice. 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: In rodents the receptor is what releases the two gut hormones; delete it and the response goes. organism: Rat and mouse tissue_or_cell_type: Colon experimental_model: Wistar rats, C57BL6 mice and FFA2 knockout mice, with colonic crypt cultures and portal vein sampling limitations: Establishes the receptor-to-hormone step in rodents using propionate rather than acetate. The knockout is the strength of the design. exposure: Propionate applied to colonic crypt cultures and infused into the colon, with FFA2 deletion as the test of mediation evidence_span: {"source_cache": "artifacts/acetate-research/25109781.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c3c934644f9308be7b2c26f969858debd0d1dbf19bee7e307e529d392fe135d6", "start_char": 0, "end_char": 1621, "text_sha256": "c3c934644f9308be7b2c26f969858debd0d1dbf19bee7e307e529d392fe135d6"} [acetate-p25109781] The short chain fatty acid propionate stimulates GLP-1 and PYY secretion via free fatty acid receptor 2 in rodents. (2015). https://pubmed.ncbi.nlm.nih.gov/25109781/ DOI: 10.1038/ijo.2014.153

evidence_access

Primary abstract

experimental_model

Human receptor expressed in yeast, mammalian cells and oocyte signaling systems.

limitations

Receptor activation alone does not establish a downstream clinical effect.

nutrient_topic

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

plain_language

One cell-surface receptor detects short-chain fatty acids.

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 502–508

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human receptor expressed in yeast, mammalian cells and oocyte signaling systems. · source_derived_draft · unverified_draft

## butyrate-ffar2-agonist One cell-surface receptor detects short-chain fatty acids. Butyrate activated human GPR43/FFAR2 in the receptor-deorphanization assays. Model: Human receptor expressed in yeast, mammalian cells and oocyte signaling systems. Limitations: Receptor activation alone does not establish a downstream clinical effect. 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

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

Acetate is not only fuel; it is the signal that identified this receptor.

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 225–236

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-acetate-activates-ffar2 The acetate anion was identified as an agonist of human GPR43 during ligand bank screening in yeast and confirmed after transient transfection using calcium mobilisation and GTP-gamma-S binding assays and by coexpression with GIRK potassium channels in Xenopus oocytes, with formate, propionate, butyrate and pentanoate also showing agonist activity. 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: Acetate is not only fuel; it is the signal that identified this receptor. 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

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

The natural fatty acids are weak at this receptor; a synthetic drug is hundreds of times stronger.

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 355–366

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-weak-partial-agonism Receptor studies confirmed acetate, propionate and butyrate to be low-potency partial agonists of FFAR2 compared with the synthetic agonist CFMB, which is a full agonist with roughly 750-fold higher potency than the short-chain fatty acids. 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 natural fatty acids are weak at this receptor; a synthetic drug is hundreds of times stronger. 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

evidence_span

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experimental_model

GPR43 knockout mice with B-cell and dendritic-cell coculture and retinoic acid signalling blockade

exposure

Dietary acetate or butyrate in wild-type and GPR43 knockout mice, with in vitro IgA class switching assays

limitations

A clean set of controls: butyrate did not substitute for acetate, the effect was independent of T cells, and blocking the downstream vitamin A metabolite removed it.

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

Acetate tells the gut to make the antibody that coats its own bacteria, and butyrate does not stand in for it.

primary_references

[acetate-p27966553] Microbiota metabolite short-chain fatty acid acetate promotes intestinal IgA response to microbiota which is mediated by GPR43. (2017). https://pubmed.ncbi.nlm.nih.gov/27966553/ DOI: 10.1038/mi.2016.114

tissue_or_cell_type

Intestinal mucosa

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 381–392

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GPR43 knockout mice with B-cell and dendritic-cell coculture and retinoic acid signalling blockade · source_derived_draft · unverified_draft

### acetate-acetate-iga GPR43 knockout mice had lower levels of intestinal IgA and of IgA-coated gut bacteria than wild-type mice, and feeding wild-type but not GPR43 knockout mice acetate, but not butyrate, promoted the intestinal IgA response independently of T cells. 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: Acetate tells the gut to make the antibody that coats its own bacteria, and butyrate does not stand in for it. organism: Mouse tissue_or_cell_type: Intestinal mucosa experimental_model: GPR43 knockout mice with B-cell and dendritic-cell coculture and retinoic acid signalling blockade limitations: A clean set of controls: butyrate did not substitute for acetate, the effect was independent of T cells, and blocking the downstream vitamin A metabolite removed it. exposure: Dietary acetate or butyrate in wild-type and GPR43 knockout mice, with in vitro IgA class switching assays evidence_span: {"source_cache": "artifacts/acetate-research/27966553.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac", "start_char": 0, "end_char": 1363, "text_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac"} [acetate-p27966553] Microbiota metabolite short-chain fatty acid acetate promotes intestinal IgA response to microbiota which is mediated by GPR43. (2017). https://pubmed.ncbi.nlm.nih.gov/27966553/ DOI: 10.1038/mi.2016.114