Component

Colonic epithelial cell

Colonic epithelial cell. Species, exposure and limitations are retained in each linked claim.

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

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

Where it participates (unsigned role)

  1. Hydroxycitrate did not affect the incorporation of acetate or butyrate carbon into lipids even though it inhibited colonic ATP-citrate lyase, suggesting that the short-chain fatty acid carbon used in lipid synthesis by colonocytes is not transported to the cytosol as citrate, and that colonocytes synthesise lipids by a pathway distinct from the liver.

    Human ATP-citrate lyase / ACLY → De novo lipogenesis source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/acetate-research/14608066.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b2c891f60d02b85a8f4e87f26751f1129b0445fe52fb35ca5e5e20a92d4ecc5a", "start_char": 0, "end_char": 1642, "text_sha256": "b2c891f60d02b85a8f4e87f26751f1129b0445fe52fb35ca5e5e20a92d4ecc5a"}
    experimental_model
    Rat colonic epithelial cells with competing labelled substrates and ATP-citrate lyase inhibition
    exposure
    Labelled acetate, propionate, butyrate, 3-hydroxybutyrate, glucose and glutamine, with hydroxycitrate as an ATP-citrate lyase inhibitor
    limitations
    An isolated cell measurement. Its ATP-citrate lyase result anticipates by seventeen years the in vivo finding in this collection that lipogenic acetyl-CoA can arrive without that enzyme.
    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 usual enzyme changed nothing, so the carbon was arriving another way.
    primary_references
    [acetate-p14608066] Acetate and butyrate are the major substrates for de novo lipogenesis in rat colonic epithelial cells. (2003). https://pubmed.ncbi.nlm.nih.gov/14608066/ DOI: 10.1093/jn/133.11.3509
    tissue_or_cell_type
    Colonic epithelium

    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 537–548

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat colonic epithelial cells with competing labelled substrates and ATP-citrate lyase inhibition · source_derived_draft · unverified_draft

    ### acetate-citrate-route-not-used Hydroxycitrate did not affect the incorporation of acetate or butyrate carbon into lipids even though it inhibited colonic ATP-citrate lyase, suggesting that the short-chain fatty acid carbon used in lipid synthesis by colonocytes is not transported to the cytosol as citrate, and that colonocytes synthesise lipids by a pathway distinct from the liver. 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 usual enzyme changed nothing, so the carbon was arriving another way. organism: Rat tissue_or_cell_type: Colonic epithelium experimental_model: Rat colonic epithelial cells with competing labelled substrates and ATP-citrate lyase inhibition limitations: An isolated cell measurement. Its ATP-citrate lyase result anticipates by seventeen years the in vivo finding in this collection that lipogenic acetyl-CoA can arrive without that enzyme. exposure: Labelled acetate, propionate, butyrate, 3-hydroxybutyrate, glucose and glutamine, with hydroxycitrate as an ATP-citrate lyase inhibitor evidence_span: {"source_cache": "artifacts/acetate-research/14608066.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b2c891f60d02b85a8f4e87f26751f1129b0445fe52fb35ca5e5e20a92d4ecc5a", "start_char": 0, "end_char": 1642, "text_sha256": "b2c891f60d02b85a8f4e87f26751f1129b0445fe52fb35ca5e5e20a92d4ecc5a"} [acetate-p14608066] Acetate and butyrate are the major substrates for de novo lipogenesis in rat colonic epithelial cells. (2003). https://pubmed.ncbi.nlm.nih.gov/14608066/ DOI: 10.1093/jn/133.11.3509
    Complete structured claim and evidence

  2. Acetate made a significantly larger carbon contribution to lipids than propionate, butyrate, glucose or glutamine in rat colonic epithelial cells, with butyrate and 3-hydroxybutyrate the other major contributors and glucose, glutamine and propionate making only minor contributions, and incorporation was significantly greater into phospholipids than into free fatty acids and triacylglycerides, suggesting the major role of this lipogenesis is membrane synthesis.

    Acetate → De novo lipogenesis source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/acetate-research/14608066.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b2c891f60d02b85a8f4e87f26751f1129b0445fe52fb35ca5e5e20a92d4ecc5a", "start_char": 0, "end_char": 1642, "text_sha256": "b2c891f60d02b85a8f4e87f26751f1129b0445fe52fb35ca5e5e20a92d4ecc5a"}
    experimental_model
    Rat colonic epithelial cells with competing labelled substrates and ATP-citrate lyase inhibition
    exposure
    Labelled acetate, propionate, butyrate, 3-hydroxybutyrate, glucose and glutamine, with hydroxycitrate as an ATP-citrate lyase inhibitor
    limitations
    An isolated cell measurement. Its ATP-citrate lyase result anticipates by seventeen years the in vivo finding in this collection that lipogenic acetyl-CoA can arrive without that enzyme.
    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 cells lining the colon build their membranes mostly out of acetate, not out of glucose.
    primary_references
    [acetate-p14608066] Acetate and butyrate are the major substrates for de novo lipogenesis in rat colonic epithelial cells. (2003). https://pubmed.ncbi.nlm.nih.gov/14608066/ DOI: 10.1093/jn/133.11.3509
    tissue_or_cell_type
    Colonic epithelium

    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 524–535

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat colonic epithelial cells with competing labelled substrates and ATP-citrate lyase inhibition · source_derived_draft · unverified_draft

    ### acetate-colonocyte-prefers-acetate Acetate made a significantly larger carbon contribution to lipids than propionate, butyrate, glucose or glutamine in rat colonic epithelial cells, with butyrate and 3-hydroxybutyrate the other major contributors and glucose, glutamine and propionate making only minor contributions, and incorporation was significantly greater into phospholipids than into free fatty acids and triacylglycerides, suggesting the major role of this lipogenesis is membrane synthesis. 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 cells lining the colon build their membranes mostly out of acetate, not out of glucose. organism: Rat tissue_or_cell_type: Colonic epithelium experimental_model: Rat colonic epithelial cells with competing labelled substrates and ATP-citrate lyase inhibition limitations: An isolated cell measurement. Its ATP-citrate lyase result anticipates by seventeen years the in vivo finding in this collection that lipogenic acetyl-CoA can arrive without that enzyme. exposure: Labelled acetate, propionate, butyrate, 3-hydroxybutyrate, glucose and glutamine, with hydroxycitrate as an ATP-citrate lyase inhibitor evidence_span: {"source_cache": "artifacts/acetate-research/14608066.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b2c891f60d02b85a8f4e87f26751f1129b0445fe52fb35ca5e5e20a92d4ecc5a", "start_char": 0, "end_char": 1642, "text_sha256": "b2c891f60d02b85a8f4e87f26751f1129b0445fe52fb35ca5e5e20a92d4ecc5a"} [acetate-p14608066] Acetate and butyrate are the major substrates for de novo lipogenesis in rat colonic epithelial cells. (2003). https://pubmed.ncbi.nlm.nih.gov/14608066/ DOI: 10.1093/jn/133.11.3509
    Complete structured claim and evidence

  3. 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.

    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/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"}
    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
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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