Component

Experimental GPR43 / FFA2-deficient mouse genotype

Experimental GPR43 / FFA2-deficient mouse genotype. Species, exposure and limitations are retained in each linked claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

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What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

Where it participates (unsigned role)

  1. 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.

    Acetate → Intestinal immunoglobulin A response to the microbiota source_derived_draftungraded
    Experimental context and source evidence
    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"}
    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
    Complete structured claim and evidence

  2. 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.

    Human free fatty acid receptor 2 / FFAR2 → Fat accumulation in adipose tissue source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    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 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
    Complete structured claim and evidence

  3. 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.

    Human free fatty acid receptor 2 / FFAR2 → Plasma GLP-1 response in the specified meal or glucose challenge source_derived_draftungraded
    Experimental context and source evidence
    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"}
    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
    Complete structured claim and evidence

In the sources

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