Acetate

evidence_access

Primary abstract

experimental_model

Human-fecal bacterial isolates and 13C-acetate tracing.

limitations

This culture fraction is not a universal human conversion percentage.

nutrient_topic

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

plain_language

One bacterium’s fermentation product can become another product’s carbon source.

primary_references

Contribution of acetate to butyrate formation by human faecal bacteria. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15182395/ · DOI 10.1079/BJN20041150

Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 54–60

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human-fecal bacterial isolates and 13C-acetate tracing. · source_derived_draft · unverified_draft

## butyrate-acetate-carbon One bacterium’s fermentation product can become another product’s carbon source. Isotope tracing showed external acetate supplied 85–90% of butyrate carbon in the tested F. prausnitzii and Roseburia cultures supplied with 60 mM acetate and 10 mM glucose. Model: Human-fecal bacterial isolates and 13C-acetate tracing. Limitations: This culture fraction is not a universal human conversion percentage. Evidence access: Primary abstract Contribution of acetate to butyrate formation by human faecal bacteria. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15182395/ · DOI 10.1079/BJN20041150

evidence_access

Primary abstract

experimental_model

Human stable-isotope colon-delivery study.

limitations

A study-specific tracer estimate, not a recommended acetate dose or a universal conversion fraction.

nutrient_topic

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

plain_language

Cross-feeding was detectable in humans as well as cultures.

primary_references

Systemic availability and metabolism of colonic-derived short-chain fatty acids in healthy subjects: a stable isotope study. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27510655/ · DOI 10.1113/JP272613

Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 94–100

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human stable-isotope colon-delivery study. · source_derived_draft · unverified_draft

## butyrate-human-acetate-conversion Cross-feeding was detectable in humans as well as cultures. Colon-delivered isotope tracing in 12 healthy people estimated 24% conversion of acetate into butyrate, the largest measured SCFA interconversion. Model: Human stable-isotope colon-delivery study. Limitations: A study-specific tracer estimate, not a recommended acetate dose or a universal conversion fraction. Evidence access: Primary abstract Systemic availability and metabolism of colonic-derived short-chain fatty acids in healthy subjects: a stable isotope study. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27510655/ · DOI 10.1113/JP272613

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

Acetate and butyrate released the hormone from the isolated gut; propionate did not.

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 329–340

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-acetate-glp1-perfused Luminal and especially vascular infusion of acetate and butyrate significantly increased colonic GLP-1 secretion and to a minor extent PYY secretion in the isolated perfused rat colon, but only after enhancement of intracellular cAMP, while propionate affected neither GLP-1 nor PYY by either route. 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 and butyrate released the hormone from the isolated gut; propionate did not. 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

evidence_span

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experimental_model

In vivo stable-isotope labelling in mice, with primary hippocampal neurons and behavioural testing

exposure

Labelled alcohol or heavy-labelled acetate administered in vivo, with ACSS2 inhibition and deletion

limitations

Isotope labelling traces the actual carbon atoms onto histones, which is stronger than correlating acetylation with exposure. A mouse study; the fetal result is a single reported exposure.

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 outside the neuron switches on the genes of learning, and blocking the enzyme that uses it blocks the learning too.

primary_references

[acetate-p31645761] Alcohol metabolism contributes to brain histone acetylation. (2019). https://pubmed.ncbi.nlm.nih.gov/31645761/ DOI: 10.1038/s41586-019-1700-7

tissue_or_cell_type

Brain and gestating fetus

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 641–652

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In vivo stable-isotope labelling in mice, with primary hippocampal neurons and behavioural testing · source_derived_draft · unverified_draft

### acetate-acetate-learning-programs In isolated primary hippocampal neurons ex vivo, extracellular acetate induced transcriptional programs related to learning and memory which were sensitive to ACSS2 inhibition, and alcohol-related associative learning was shown to require ACSS2 in vivo. 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 outside the neuron switches on the genes of learning, and blocking the enzyme that uses it blocks the learning too. organism: Mouse tissue_or_cell_type: Brain and gestating fetus experimental_model: In vivo stable-isotope labelling in mice, with primary hippocampal neurons and behavioural testing limitations: Isotope labelling traces the actual carbon atoms onto histones, which is stronger than correlating acetylation with exposure. A mouse study; the fetal result is a single reported exposure. exposure: Labelled alcohol or heavy-labelled acetate administered in vivo, with ACSS2 inhibition and deletion evidence_span: {"source_cache": "artifacts/acetate-research/31645761.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a7a812a410fd8be3bad8512ab46d4b8a7fd3329d1552ee30965b66860eeb2b2f", "start_char": 0, "end_char": 1646, "text_sha256": "a7a812a410fd8be3bad8512ab46d4b8a7fd3329d1552ee30965b66860eeb2b2f"} [acetate-p31645761] Alcohol metabolism contributes to brain histone acetylation. (2019). https://pubmed.ncbi.nlm.nih.gov/31645761/ DOI: 10.1038/s41586-019-1700-7

evidence_span

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experimental_model

In vivo carbon-11 acetate PET-CT in rodents with carbon-13 high-resolution magic-angle-spinning spectroscopy

exposure

Colonic and intraperitoneal acetate, and carbon-13 labelled fermentable carbohydrate

limitations

Traces the molecule from colon to brain and then measures what it does there. The appetite endpoint is rodent, and intraperitoneal administration is not a dietary exposure.

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

Rodent

plain_language

Acetate made by gut bacteria reaches the brain and can be measured there.

primary_references

[acetate-p24781306] The short-chain fatty acid acetate reduces appetite via a central homeostatic mechanism. (2014). https://pubmed.ncbi.nlm.nih.gov/24781306/ DOI: 10.1038/ncomms4611

tissue_or_cell_type

Colon, blood-brain barrier and hypothalamus

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 706–717

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In vivo carbon-11 acetate PET-CT in rodents with carbon-13 high-resolution magic-angle-spinning spectroscopy · source_derived_draft · unverified_draft

### acetate-acetate-reaches-brain In vivo carbon-11 acetate PET-CT showed that colonic acetate crosses the blood-brain barrier and is taken up by the brain, and carbon-13 magic-angle-spinning spectroscopy showed that carbon-13 acetate from fermentation of labelled carbohydrate in the colon increases hypothalamic carbon-13 acetate above baseline levels. 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 made by gut bacteria reaches the brain and can be measured there. organism: Rodent tissue_or_cell_type: Colon, blood-brain barrier and hypothalamus experimental_model: In vivo carbon-11 acetate PET-CT in rodents with carbon-13 high-resolution magic-angle-spinning spectroscopy limitations: Traces the molecule from colon to brain and then measures what it does there. The appetite endpoint is rodent, and intraperitoneal administration is not a dietary exposure. exposure: Colonic and intraperitoneal acetate, and carbon-13 labelled fermentable carbohydrate evidence_span: {"source_cache": "artifacts/acetate-research/24781306.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4a1cc3cf5135e5856a281cd391c82611caa57afa2f837b0343cf048bb2c11e97", "start_char": 0, "end_char": 1135, "text_sha256": "4a1cc3cf5135e5856a281cd391c82611caa57afa2f837b0343cf048bb2c11e97"} [acetate-p24781306] The short-chain fatty acid acetate reduces appetite via a central homeostatic mechanism. (2014). https://pubmed.ncbi.nlm.nih.gov/24781306/ DOI: 10.1038/ncomms4611

evidence_span

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experimental_model

In vivo carbon-11 acetate PET-CT in rodents with carbon-13 high-resolution magic-angle-spinning spectroscopy

exposure

Colonic and intraperitoneal acetate, and carbon-13 labelled fermentable carbohydrate

limitations

Traces the molecule from colon to brain and then measures what it does there. The appetite endpoint is rodent, and intraperitoneal administration is not a dietary exposure.

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

Rodent

plain_language

Once there it changes the hypothalamic circuits that set hunger.

primary_references

[acetate-p24781306] The short-chain fatty acid acetate reduces appetite via a central homeostatic mechanism. (2014). https://pubmed.ncbi.nlm.nih.gov/24781306/ DOI: 10.1038/ncomms4611

tissue_or_cell_type

Colon, blood-brain barrier and hypothalamus

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 719–730

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In vivo carbon-11 acetate PET-CT in rodents with carbon-13 high-resolution magic-angle-spinning spectroscopy · source_derived_draft · unverified_draft

### acetate-acetate-suppresses-appetite Intraperitoneal acetate resulted in appetite suppression and hypothalamic neuronal activation patterning, was associated with activation of acetyl-CoA carboxylase and changes in the expression profiles of regulatory neuropeptides that favour appetite suppression, and regionally increased the labelling of the glutamate-glutamine and GABA neuroglial cycles, suggesting a direct role for acetate in central appetite regulation. 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: Once there it changes the hypothalamic circuits that set hunger. organism: Rodent tissue_or_cell_type: Colon, blood-brain barrier and hypothalamus experimental_model: In vivo carbon-11 acetate PET-CT in rodents with carbon-13 high-resolution magic-angle-spinning spectroscopy limitations: Traces the molecule from colon to brain and then measures what it does there. The appetite endpoint is rodent, and intraperitoneal administration is not a dietary exposure. exposure: Colonic and intraperitoneal acetate, and carbon-13 labelled fermentable carbohydrate evidence_span: {"source_cache": "artifacts/acetate-research/24781306.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4a1cc3cf5135e5856a281cd391c82611caa57afa2f837b0343cf048bb2c11e97", "start_char": 0, "end_char": 1135, "text_sha256": "4a1cc3cf5135e5856a281cd391c82611caa57afa2f837b0343cf048bb2c11e97"} [acetate-p24781306] The short-chain fatty acid acetate reduces appetite via a central homeostatic mechanism. (2014). https://pubmed.ncbi.nlm.nih.gov/24781306/ DOI: 10.1038/ncomms4611

evidence_span

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experimental_model

Drosophila mutagenesis and RNA interference in enteroendocrine cells of the anterior midgut

exposure

Dietary acetate with disruption of a monocarboxylic acid transporter, of histone deacetylation, and of the Tip60 acetyltransferase

limitations

This is a fly study. The mammalian relevance is the authors’ statement that the Tip60-steroid hormone axis is conserved, not a mammalian measurement.

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

Drosophila

plain_language

In the fly, bacterial acetate switches on the gut immune pathway, and the same switch also controls how much fat the gut makes.

primary_references

[acetate-p34107298] Microbiota-derived acetate activates intestinal innate immunity via the Tip60 histone acetyltransferase complex. (2021). https://pubmed.ncbi.nlm.nih.gov/34107298/ DOI: 10.1016/j.immuni.2021.05.017

tissue_or_cell_type

Anterior midgut

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 680–691

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Drosophila mutagenesis and RNA interference in enteroendocrine cells of the anterior midgut · source_derived_draft · unverified_draft

### acetate-acetate-tip60-immunity Microbe-derived acetate activated the Drosophila immunodeficiency pathway in a subset of enteroendocrine cells of the anterior midgut, where the pathway co-regulates expression of antimicrobial and enteroendocrine peptides including tachykinin, a repressor of intestinal lipid 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: In the fly, bacterial acetate switches on the gut immune pathway, and the same switch also controls how much fat the gut makes. organism: Drosophila tissue_or_cell_type: Anterior midgut experimental_model: Drosophila mutagenesis and RNA interference in enteroendocrine cells of the anterior midgut limitations: This is a fly study. The mammalian relevance is the authors’ statement that the Tip60-steroid hormone axis is conserved, not a mammalian measurement. exposure: Dietary acetate with disruption of a monocarboxylic acid transporter, of histone deacetylation, and of the Tip60 acetyltransferase evidence_span: {"source_cache": "artifacts/acetate-research/34107298.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4e5644412d174b2512ecf9cedea282b022d647b1b8a82f693a8f389da991425a", "start_char": 0, "end_char": 1179, "text_sha256": "4e5644412d174b2512ecf9cedea282b022d647b1b8a82f693a8f389da991425a"} [acetate-p34107298] Microbiota-derived acetate activates intestinal innate immunity via the Tip60 histone acetyltransferase complex. (2021). https://pubmed.ncbi.nlm.nih.gov/34107298/ DOI: 10.1016/j.immuni.2021.05.017

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 works by switching on the enzyme that turns vitamin A into its active form; block that and the effect is gone.

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 394–405

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-vitamin-a-route Acetate promoted B-cell IgA class switching and IgA production in vitro in the presence of wild-type but not GPR43 knockout dendritic cells, and mechanistically acetate induced dendritic-cell expression of Aldh1a2, which converts vitamin A into retinoic acid, with blockade of retinoic acid signalling inhibiting the acetate-induced IgA production. 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 works by switching on the enzyme that turns vitamin A into its active form; block that and the effect is gone. 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

evidence_span

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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

evidence_span

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experimental_model

KK-Ay diabetic mice fed for 8 weeks, with rat hepatocyte experiments

exposure

0.3% dietary acetic acid for 8 weeks; sodium acetate as neutralised acetic acid applied to rat hepatocytes

limitations

The hepatocyte arm used the neutralised salt and still activated AMPK, which does not sit easily beside the human finding that the acid rather than the salt lowered glucose. Both are recorded.

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 and rat cells

plain_language

The neutralised salt switched on the liver cell energy sensor directly.

primary_references

[acetate-p16630552] Acetic acid activates hepatic AMPK and reduces hyperglycemia in diabetic KK-A(y) mice. (2006). https://pubmed.ncbi.nlm.nih.gov/16630552/ DOI: 10.1016/j.bbrc.2006.03.176

tissue_or_cell_type

Liver

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 420–431

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KK-Ay diabetic mice fed for 8 weeks, with rat hepatocyte experiments · source_derived_draft · unverified_draft

### acetate-sodium-acetate-hepatocyte Sodium acetate, in the form of neutralised acetic acid, directly activated AMPK and lowered the expression of genes such as glucose-6-phosphatase and sterol regulatory element binding protein 1 in rat hepatocytes, leading the authors to conclude that the hypoglycaemic effect might be due to activation of AMPK in 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: The neutralised salt switched on the liver cell energy sensor directly. organism: Mouse and rat cells tissue_or_cell_type: Liver experimental_model: KK-Ay diabetic mice fed for 8 weeks, with rat hepatocyte experiments limitations: The hepatocyte arm used the neutralised salt and still activated AMPK, which does not sit easily beside the human finding that the acid rather than the salt lowered glucose. Both are recorded. exposure: 0.3% dietary acetic acid for 8 weeks; sodium acetate as neutralised acetic acid applied to rat hepatocytes evidence_span: {"source_cache": "artifacts/acetate-research/16630552.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8e99fe94e17c850602d0da9607212293dfc8d773e356b73ef37c4b071bbeabea", "start_char": 0, "end_char": 914, "text_sha256": "8e99fe94e17c850602d0da9607212293dfc8d773e356b73ef37c4b071bbeabea"} [acetate-p16630552] Acetic acid activates hepatic AMPK and reduces hyperglycemia in diabetic KK-A(y) mice. (2006). https://pubmed.ncbi.nlm.nih.gov/16630552/ DOI: 10.1016/j.bbrc.2006.03.176

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

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

false

evidence_location

BioC text lines 11, 51; Fig. 2A–B

experimental_model

ACLY and/or AceCS1 siRNA with acetate supplementation

exposure

0, 1 or 5 mM acetate for 24 hours before lysis after siRNA treatment.

limitations

The authors identify this acetate supply as supraphysiologic; it is not a dietary recommendation and does not show rescue of an absent CoA pool. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.

nutrient_topic

Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)

organism

Homo sapiens

plain_language

A second acetyl-CoA-producing route could compensate when enough acetate was supplied.

primary_references

[b5-met-chromatin2009] ATP-citrate lyase links cellular metabolism to histone acetylation. (2009). https://pubmed.ncbi.nlm.nih.gov/19461003/ DOI: 10.1126/science.1164097

tissue_or_cell_type

HCT116 cells

trigger_kind

machinery_impairment Imported condition classification; unverified.

Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1005–1017

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · ACLY and/or AceCS1 siRNA with acetate supplementation · source_derived_draft · unverified_draft

### b5-met-acetate-acss2-histone-rescue Extracellular acetate restored histone acetylation in ACLY-silenced HCT116 cells in a dose-dependent manner that required AceCS1, now named ACSS2. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second acetyl-CoA-producing route could compensate when enough acetate was supplied. organism: Homo sapiens tissue_or_cell_type: HCT116 cells experimental_model: ACLY and/or AceCS1 siRNA with acetate supplementation limitations: The authors identify this acetate supply as supraphysiologic; it is not a dietary recommendation and does not show rescue of an absent CoA pool. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: 0, 1 or 5 mM acetate for 24 hours before lysis after siRNA treatment. cross_nutrient: false evidence_location: BioC text lines 11, 51; Fig. 2A–B [b5-met-chromatin2009] ATP-citrate lyase links cellular metabolism to histone acetylation. (2009). https://pubmed.ncbi.nlm.nih.gov/19461003/ DOI: 10.1126/science.1164097

evidence_span

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experimental_model

Drosophila mutagenesis and RNA interference in enteroendocrine cells of the anterior midgut

exposure

Dietary acetate with disruption of a monocarboxylic acid transporter, of histone deacetylation, and of the Tip60 acetyltransferase

limitations

This is a fly study. The mammalian relevance is the authors’ statement that the Tip60-steroid hormone axis is conserved, not a mammalian measurement.

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

Drosophila

plain_language

Acetate has to be carried inside the cell and turned into a chromatin mark; it is not read at the cell surface.

primary_references

[acetate-p34107298] Microbiota-derived acetate activates intestinal innate immunity via the Tip60 histone acetyltransferase complex. (2021). https://pubmed.ncbi.nlm.nih.gov/34107298/ DOI: 10.1016/j.immuni.2021.05.017

tissue_or_cell_type

Anterior midgut

transport_effect

raises The transporter was required for dietary acetate to reach the intracellular acetyl-CoA route.

transport_pool

the intracellular acetate pool The transporter was required for dietary acetate to reach the intracellular acetyl-CoA route.

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 693–704

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Drosophila mutagenesis and RNA interference in enteroendocrine cells of the anterior midgut · source_derived_draft · unverified_draft

### acetate-acetate-must-enter Mutagenesis and RNA interference revealed that the putative monocarboxylic acid transporter Tarag was essential for enhancement of immunodeficiency pathway signalling by dietary acetate, and reduced expression of the histone acetyltransferase Tip60 decreased that signalling and blocked rescue by dietary acetate and by other sources of intracellular acetyl-CoA, while interference with histone deacetylation augmented transcription of ecdysone-regulated genes including pathway targets. 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 has to be carried inside the cell and turned into a chromatin mark; it is not read at the cell surface. organism: Drosophila tissue_or_cell_type: Anterior midgut experimental_model: Drosophila mutagenesis and RNA interference in enteroendocrine cells of the anterior midgut limitations: This is a fly study. The mammalian relevance is the authors’ statement that the Tip60-steroid hormone axis is conserved, not a mammalian measurement. exposure: Dietary acetate with disruption of a monocarboxylic acid transporter, of histone deacetylation, and of the Tip60 acetyltransferase evidence_span: {"source_cache": "artifacts/acetate-research/34107298.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4e5644412d174b2512ecf9cedea282b022d647b1b8a82f693a8f389da991425a", "start_char": 0, "end_char": 1179, "text_sha256": "4e5644412d174b2512ecf9cedea282b022d647b1b8a82f693a8f389da991425a"} [acetate-p34107298] Microbiota-derived acetate activates intestinal innate immunity via the Tip60 histone acetyltransferase complex. (2021). https://pubmed.ncbi.nlm.nih.gov/34107298/ DOI: 10.1016/j.immuni.2021.05.017

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

Randomised six-meal crossover in five healthy subjects, with ultrasonographic gastric emptying in four others

exposure

1 g acetic acid as native vinegar, or the same vinegar neutralised to pH 6.0 with sodium bicarbonate, each on a lettuce and olive oil meal with or without 50 g carbohydrate as white bread

limitations

The decisive control in this collection: it separates the acid from its sodium salt and measures gastric emptying directly in the same design. Five subjects for the glucose arm and four for the ultrasound arm is very small.

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

plain_language

Swallowing the acid does put acetate into the blood, but less of it than the neutralised salt does.

primary_references

[acetate-p7796781] Effect of neutralized and native vinegar on blood glucose and acetate responses to a mixed meal in healthy subjects. (1995). https://pubmed.ncbi.nlm.nih.gov/7796781/

tissue_or_cell_type

Whole body and stomach

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 69–80

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised six-meal crossover in five healthy subjects, with ultrasonographic gastric emptying in four others · source_derived_draft · unverified_draft

### acetate-ingestion-to-plasma-acetate Acetate concentrations were measured in arterialized capillary blood before and until 95 minutes after meals containing acetic acid as vinegar or sodium acetate as neutralised vinegar, and the blood acetate response over 95 minutes was markedly reduced after the acetic acid meals compared with the sodium acetate meals. 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: Swallowing the acid does put acetate into the blood, but less of it than the neutralised salt does. organism: Human tissue_or_cell_type: Whole body and stomach experimental_model: Randomised six-meal crossover in five healthy subjects, with ultrasonographic gastric emptying in four others limitations: The decisive control in this collection: it separates the acid from its sodium salt and measures gastric emptying directly in the same design. Five subjects for the glucose arm and four for the ultrasound arm is very small. exposure: 1 g acetic acid as native vinegar, or the same vinegar neutralised to pH 6.0 with sodium bicarbonate, each on a lettuce and olive oil meal with or without 50 g carbohydrate as white bread evidence_span: {"source_cache": "artifacts/acetate-research/7796781.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "88f9eba4673a81b8a0d190d3303d1d43ba908e457cc8794a457c962074c7d60f", "start_char": 0, "end_char": 1533, "text_sha256": "88f9eba4673a81b8a0d190d3303d1d43ba908e457cc8794a457c962074c7d60f"} [acetate-p7796781] Effect of neutralized and native vinegar on blood glucose and acetate responses to a mixed meal in healthy subjects. (1995). https://pubmed.ncbi.nlm.nih.gov/7796781/

dose

Bolus 2 g/kg labeled fructose plus 2 g/kg glucose; interventions specified by claim

duration

Acute isotope sampling up to 6 h

evidence_access

Primary full-text methods/results and metadata inspected.

evidence_scope

literature_reviewed; source-specific curation

experimental_model

Wild-type mice, microbiota depletion and liver Acss2-silencing experiments

exposure_scope

Component mixture

limitations

Carbon tracing supports microbial acetate supply; antibiotic depletion is not a clinical recommendation and microbiota effects are not universal across diets.

nutrient_topic

HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS

organism

Wild-type mice, microbiota depletion and liver Acss2-silencing experiments

plain_language

Mouse tracer experiments identified gut-microbial acetate derived from ingested fructose.

primary_references

Dietary fructose feeds hepatic lipogenesis via microbiota-derived acetate. (2020). https://pubmed.ncbi.nlm.nih.gov/32214246/ DOI: 10.1038/s41586-020-2101-7

route

Oral gavage and experimental microbiota/gene perturbation

tissue

Portal acetate and hepatic fatty-acid labeling

High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 209–219

Original AI-assisted curation of twenty primary studies and official FDA composition information, with one reused canonical glucose-transport claim. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Wild-type mice, microbiota depletion and liver Acss2-silencing experiments · source_derived_draft · unverified_draft

## hfcs-microbial-acetate Mouse tracer experiments identified gut-microbial acetate derived from ingested fructose. Model/species: Wild-type mice, microbiota depletion and liver Acss2-silencing experiments Tissue: Portal acetate and hepatic fatty-acid labeling Exposure: Bolus 2 g/kg labeled fructose plus 2 g/kg glucose; interventions specified by claim Route: Oral gavage and experimental microbiota/gene perturbation Duration: Acute isotope sampling up to 6 h Exposure scope: Component mixture Limits: Carbon tracing supports microbial acetate supply; antibiotic depletion is not a clinical recommendation and microbiota effects are not universal across diets. Reference: Dietary fructose feeds hepatic lipogenesis via microbiota-derived acetate. (2020). https://pubmed.ncbi.nlm.nih.gov/32214246/ DOI: 10.1038/s41586-020-2101-7 Access: Primary full-text methods/results and metadata inspected.

evidence_span

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experimental_model

M-SHIME simulated colons with four donor microbiotas

exposure

Carrot RG-I extract, 3 g/day for three weeks in the model

limitations

No human host received this regimen in this experiment. Donor-specific cultures and product composition limit extrapolation.

nutrient_topic

Pectin research collection; topical membership is not evidence of a direct dietary effect. · Pectin, structurally heterogeneous plant polysaccharides

organism

Human fecal microbial communities in vitro

plain_language

This particular extract supported microbial production of acetate in simulated colons.

primary_references

[pectin-p34683463] Consistent Prebiotic Effects of Carrot RG-I on the Gut Microbiota of Four Human Adult Donors in the SHIME® Model despite Baseline Individual Variability. (2021). https://pubmed.ncbi.nlm.nih.gov/34683463/ DOI: 10.3390/microorganisms9102142

tissue_or_cell_type

Simulated colonic compartments

Pectin: metabolism, signaling and nutrient connections (2026-09-17) · lines 906–917

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · M-SHIME simulated colons with four donor microbiotas · source_derived_draft · unverified_draft

### pectin-crgi-acetate The carrot RG-I model intervention increased acetate by a reported 21.1 mM. Condition category: normal nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This particular extract supported microbial production of acetate in simulated colons. organism: Human fecal microbial communities in vitro tissue_or_cell_type: Simulated colonic compartments experimental_model: M-SHIME simulated colons with four donor microbiotas limitations: No human host received this regimen in this experiment. Donor-specific cultures and product composition limit extrapolation. exposure: Carrot RG-I extract, 3 g/day for three weeks in the model evidence_span: {"source_cache": "artifacts/pectin-research/34683463.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "38a179d5d001092c0d9595bb3d93ae4fcf8780bb7ae6286e0edfd27971c2aabc", "start_char": 0, "end_char": 1830, "text_sha256": "38a179d5d001092c0d9595bb3d93ae4fcf8780bb7ae6286e0edfd27971c2aabc"} [pectin-p34683463] Consistent Prebiotic Effects of Carrot RG-I on the Gut Microbiota of Four Human Adult Donors in the SHIME® Model despite Baseline Individual Variability. (2021). https://pubmed.ncbi.nlm.nih.gov/34683463/ DOI: 10.3390/microorganisms9102142

evidence_access

Primary abstract

experimental_model

Anaerobic human-fecal isolates; enzyme assays and gene analysis.

limitations

A defined isolate panel is not a census of every human microbiome.

nutrient_topic

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

plain_language

Many tested gut bacteria used acetate-linked CoA transfer to finish butyrate synthesis.

primary_references

Restricted distribution of the butyrate kinase pathway among butyrate-producing bacteria from the human colon. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15028695/ · DOI 10.1128/JB.186.7.2099-2106.2004

Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 38–44

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Anaerobic human-fecal isolates; enzyme assays and gene analysis. · source_derived_draft · unverified_draft

## butyrate-coa-transferase-route Many tested gut bacteria used acetate-linked CoA transfer to finish butyrate synthesis. Butyryl-CoA:acetate CoA-transferase activity was detected in all 38 human-fecal butyrate-producing isolates examined, supporting this terminal route to butyrate. Model: Anaerobic human-fecal isolates; enzyme assays and gene analysis. Limitations: A defined isolate panel is not a census of every human microbiome. Evidence access: Primary abstract Restricted distribution of the butyrate kinase pathway among butyrate-producing bacteria from the human colon. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15028695/ · DOI 10.1128/JB.186.7.2099-2106.2004

availability_state

biomarker_context Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

Human stable-isotope pharmacokinetic study.

limitations

Specific to colonic delivery and study conditions; does not quantify oral immediate-release, rectal or injected exposure.

nutrient_topic

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

plain_language

Most colon-delivered butyrate did not reach the general circulation unchanged.

primary_references

Systemic availability and metabolism of colonic-derived short-chain fatty acids in healthy subjects: a stable isotope study. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27510655/ · DOI 10.1113/JP272613

trigger_kind

biomarker_context Imported condition classification; unverified.

Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 142–148

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human stable-isotope pharmacokinetic study. · source_derived_draft · unverified_draft

## butyrate-systemic-availability Most colon-delivered butyrate did not reach the general circulation unchanged. In 12 healthy subjects receiving isotope-labeled SCFAs in colon-release capsules, systemic availability was approximately 2% for butyrate, compared with 9% propionate and 36% acetate. Model: Human stable-isotope pharmacokinetic study. Limitations: Specific to colonic delivery and study conditions; does not quantify oral immediate-release, rectal or injected exposure. Evidence access: Primary abstract Systemic availability and metabolism of colonic-derived short-chain fatty acids in healthy subjects: a stable isotope study. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27510655/ · DOI 10.1113/JP272613

evidence_span

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experimental_model

Fixed-sequence crossover intervention with three granolas over three days each

exposure

Granola containing low, medium or high cereal beta-glucan, given in that order

limitations

Fourteen completers, a fixed sequence rather than randomised order, and granolas that differed in other constituents including inulin. Short-chain fatty acids were measured in blood while faecal samples were used for the microbiota.

nutrient_topic

Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan

organism

Human

plain_language

Three days of a cereal glucan raised two of the three main fermentation acids in the blood.

primary_references

[bg-p35578615] A Three-Day Intervention With Granola Containing Cereal Beta-Glucan Improves Glycemic Response and Changes the Gut Microbiota in Healthy Individuals: A Crossover Study. (2022). https://pubmed.ncbi.nlm.nih.gov/35578615/ DOI: 10.3389/fnut.2022.796362

tissue_or_cell_type

Blood and faecal microbiota

Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 645–656

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fixed-sequence crossover intervention with three granolas over three days each · source_derived_draft · unverified_draft

### bg-circulating-scfa-rise-with-granola A three-day intervention with granola containing cereal beta-glucan improved the glycemic response and changed the gut microbiota, with circulating acetate and butyrate increasing while propionate did not, in a study in which participants consumed granolas of differing beta-glucan content in fixed sequence and in which the granolas also differed in other constituents. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: Three days of a cereal glucan raised two of the three main fermentation acids in the blood. organism: Human tissue_or_cell_type: Blood and faecal microbiota experimental_model: Fixed-sequence crossover intervention with three granolas over three days each limitations: Fourteen completers, a fixed sequence rather than randomised order, and granolas that differed in other constituents including inulin. Short-chain fatty acids were measured in blood while faecal samples were used for the microbiota. exposure: Granola containing low, medium or high cereal beta-glucan, given in that order evidence_span: {"source_cache": "artifacts/glucan-research/35578615.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "df79afd1ef3d79ffee2a9da5f5f7e487f296cca7e9ccfcda177266b08efed747", "start_char": 0, "end_char": 2197, "text_sha256": "df79afd1ef3d79ffee2a9da5f5f7e487f296cca7e9ccfcda177266b08efed747"} [bg-p35578615] A Three-Day Intervention With Granola Containing Cereal Beta-Glucan Improves Glycemic Response and Changes the Gut Microbiota in Healthy Individuals: A Crossover Study. (2022). https://pubmed.ncbi.nlm.nih.gov/35578615/ DOI: 10.3389/fnut.2022.796362

evidence_span

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experimental_model

Time-course Western blot analysis of brain and liver histone acetylation in rats after a single oral dose

exposure

A single oral dose of 6 g/kg glyceryl triacetate, an acetate precursor

limitations

A large single dose of a precursor, not dietary acetate. The mechanism is loss of deacetylation rather than added acetylation, and only some marks moved.

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

Three specific marks on brain histones went up for a few hours; the rest, and the liver, did not move.

primary_references

[acetate-p21359531] Acetate supplementation increases brain histone acetylation and inhibits histone deacetylase activity and expression. (2011). https://pubmed.ncbi.nlm.nih.gov/21359531/ DOI: 10.1007/s11010-011-0751-3

tissue_or_cell_type

Brain and liver

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 654–665

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-course Western blot analysis of brain and liver histone acetylation in rats after a single oral dose · source_derived_draft · unverified_draft

### acetate-acetate-brain-histones A single oral dose of glyceryl triacetate increased the acetylation state of brain histone H4 at lysine 8 at 2 and 4 hours, histone H4 at lysine 16 at 4 and 24 hours, and histone H3 at lysine 9 at 4 hours, with no changes in other forms of brain or liver H3 and H4 acetylation state at any time measured. 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: Three specific marks on brain histones went up for a few hours; the rest, and the liver, did not move. organism: Rat tissue_or_cell_type: Brain and liver experimental_model: Time-course Western blot analysis of brain and liver histone acetylation in rats after a single oral dose limitations: A large single dose of a precursor, not dietary acetate. The mechanism is loss of deacetylation rather than added acetylation, and only some marks moved. exposure: A single oral dose of 6 g/kg glyceryl triacetate, an acetate precursor evidence_span: {"source_cache": "artifacts/acetate-research/21359531.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a60e30b6fa78f5fc4d9da17279ec1ecc29dd20939df5771ba26996900102014b", "start_char": 0, "end_char": 1456, "text_sha256": "a60e30b6fa78f5fc4d9da17279ec1ecc29dd20939df5771ba26996900102014b"} [acetate-p21359531] Acetate supplementation increases brain histone acetylation and inhibits histone deacetylase activity and expression. (2011). https://pubmed.ncbi.nlm.nih.gov/21359531/ DOI: 10.1007/s11010-011-0751-3

evidence_span

{"source_cache": "artifacts/acetate-research/7762627.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "343ba052925b754982d178cee1a1c2e3e0a3d1e940e6dd349989c7d6c2704f76", "start_char": 0, "end_char": 1730, "text_sha256": "343ba052925b754982d178cee1a1c2e3e0a3d1e940e6dd349989c7d6c2704f76"}

experimental_model

Eight human subjects infused with sodium acetate at rest and during cycling, with muscle biopsies

exposure

400 mmol sodium acetate infused over 20 min rest, 5 min cycling at 40% and 15 min at 80% of maximal oxygen uptake, against a 400 mmol sodium bicarbonate control two weeks later

limitations

A direct human measurement with a matched sodium control. The effect was present at rest and absent during exercise, so it is not a general property of raised acetate.

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

plain_language

Raising blood acetate in people switched down the enzyme that commits glucose to being burned.

primary_references

[acetate-p7762627] Skeletal muscle pyruvate dehydrogenase activity during acetate infusion in humans. (1995). https://pubmed.ncbi.nlm.nih.gov/7762627/ DOI: 10.1152/ajpendo.1995.268.5.e1007

tissue_or_cell_type

Skeletal muscle

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 485–496

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Eight human subjects infused with sodium acetate at rest and during cycling, with muscle biopsies · source_derived_draft · unverified_draft

### acetate-acetate-suppresses-pdh Acetate infusion increased muscle acetyl-CoA, citrate and acetylcarnitine, and resting active-form pyruvate dehydrogenase declined during 20 minutes of acetate infusion from 0.37 to 0.16 mmol per minute per kg wet weight, coinciding with an elevation in the acetyl-CoA to free CoA ratio from 0.28 to 0.73, whereas after the bicarbonate control infusion resting activity was similar to that before acetate. 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: Raising blood acetate in people switched down the enzyme that commits glucose to being burned. organism: Human tissue_or_cell_type: Skeletal muscle experimental_model: Eight human subjects infused with sodium acetate at rest and during cycling, with muscle biopsies limitations: A direct human measurement with a matched sodium control. The effect was present at rest and absent during exercise, so it is not a general property of raised acetate. exposure: 400 mmol sodium acetate infused over 20 min rest, 5 min cycling at 40% and 15 min at 80% of maximal oxygen uptake, against a 400 mmol sodium bicarbonate control two weeks later evidence_span: {"source_cache": "artifacts/acetate-research/7762627.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "343ba052925b754982d178cee1a1c2e3e0a3d1e940e6dd349989c7d6c2704f76", "start_char": 0, "end_char": 1730, "text_sha256": "343ba052925b754982d178cee1a1c2e3e0a3d1e940e6dd349989c7d6c2704f76"} [acetate-p7762627] Skeletal muscle pyruvate dehydrogenase activity during acetate infusion in humans. (1995). https://pubmed.ncbi.nlm.nih.gov/7762627/ DOI: 10.1152/ajpendo.1995.268.5.e1007

evidence_span

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experimental_model

In vivo stable-isotope labelling in mice, with primary hippocampal neurons and behavioural testing

exposure

Labelled alcohol or heavy-labelled acetate administered in vivo, with ACSS2 inhibition and deletion

limitations

Isotope labelling traces the actual carbon atoms onto histones, which is stronger than correlating acetylation with exposure. A mouse study; the fetal result is a single reported exposure.

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

Atoms from the drink end up on the proteins that package DNA in the brain.

primary_references

[acetate-p31645761] Alcohol metabolism contributes to brain histone acetylation. (2019). https://pubmed.ncbi.nlm.nih.gov/31645761/ DOI: 10.1038/s41586-019-1700-7

tissue_or_cell_type

Brain and gestating fetus

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 615–626

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In vivo stable-isotope labelling in mice, with primary hippocampal neurons and behavioural testing · source_derived_draft · unverified_draft

### acetate-alcohol-to-brain-histones Using in vivo stable-isotope labelling in mice, the metabolism of alcohol contributed to rapid acetylation of histones in the brain, in part through direct deposition of acetyl groups derived from alcohol onto histones in an ACSS2-dependent manner, and a similar direct deposition was observed when mice were injected with heavy-labelled acetate in vivo. 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: Atoms from the drink end up on the proteins that package DNA in the brain. organism: Mouse tissue_or_cell_type: Brain and gestating fetus experimental_model: In vivo stable-isotope labelling in mice, with primary hippocampal neurons and behavioural testing limitations: Isotope labelling traces the actual carbon atoms onto histones, which is stronger than correlating acetylation with exposure. A mouse study; the fetal result is a single reported exposure. exposure: Labelled alcohol or heavy-labelled acetate administered in vivo, with ACSS2 inhibition and deletion evidence_span: {"source_cache": "artifacts/acetate-research/31645761.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a7a812a410fd8be3bad8512ab46d4b8a7fd3329d1552ee30965b66860eeb2b2f", "start_char": 0, "end_char": 1646, "text_sha256": "a7a812a410fd8be3bad8512ab46d4b8a7fd3329d1552ee30965b66860eeb2b2f"} [acetate-p31645761] Alcohol metabolism contributes to brain histone acetylation. (2019). https://pubmed.ncbi.nlm.nih.gov/31645761/ DOI: 10.1038/s41586-019-1700-7

evidence_span

{"source_cache": "artifacts/acetate-research/28099844.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6df5e8ccde04ad8a222db774f6a8b1e8838ad6a1d918ff84b667d6dde57de188", "start_char": 0, "end_char": 1134, "text_sha256": "6df5e8ccde04ad8a222db774f6a8b1e8838ad6a1d918ff84b667d6dde57de188"}

experimental_model

Quantitative analysis of acetate metabolism in cultured cells under oxygen and serum limitation

exposure

Exogenous acetate with ACSS2 and ACSS1 manipulation under oxygen and serum limitation

limitations

The quantitative accounting here is the important part and it is a limiting result: demand for two-carbon units far exceeds what exogenous acetate supplies. Cultured cells at a given acetate concentration, which is not a fed human.

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

Cultured cells

plain_language

Acetate taken in from outside is mostly burned or built into fat; very little of it reaches the histones.

primary_references

[acetate-p28099844] Acetate Recapturing by Nuclear Acetyl-CoA Synthetase 2 Prevents Loss of Histone Acetylation during Oxygen and Serum Limitation. (2017). https://pubmed.ncbi.nlm.nih.gov/28099844/ DOI: 10.1016/j.celrep.2016.12.055

tissue_or_cell_type

Nucleus and cytosol

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 589–600

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Quantitative analysis of acetate metabolism in cultured cells under oxygen and serum limitation · source_derived_draft · unverified_draft

### acetate-exogenous-acetate-sparing Exogenous acetate uptake is controlled by expression of both ACSS2 and the mitochondrial ACSS1, and the mitochondrial and lipogenic demand for two-carbon acetyl units considerably exceeds the uptake of exogenous acetate, leaving it to only sparingly contribute to histone acetylation. 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 taken in from outside is mostly burned or built into fat; very little of it reaches the histones. organism: Cultured cells tissue_or_cell_type: Nucleus and cytosol experimental_model: Quantitative analysis of acetate metabolism in cultured cells under oxygen and serum limitation limitations: The quantitative accounting here is the important part and it is a limiting result: demand for two-carbon units far exceeds what exogenous acetate supplies. Cultured cells at a given acetate concentration, which is not a fed human. exposure: Exogenous acetate with ACSS2 and ACSS1 manipulation under oxygen and serum limitation evidence_span: {"source_cache": "artifacts/acetate-research/28099844.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6df5e8ccde04ad8a222db774f6a8b1e8838ad6a1d918ff84b667d6dde57de188", "start_char": 0, "end_char": 1134, "text_sha256": "6df5e8ccde04ad8a222db774f6a8b1e8838ad6a1d918ff84b667d6dde57de188"} [acetate-p28099844] Acetate Recapturing by Nuclear Acetyl-CoA Synthetase 2 Prevents Loss of Histone Acetylation during Oxygen and Serum Limitation. (2017). https://pubmed.ncbi.nlm.nih.gov/28099844/ DOI: 10.1016/j.celrep.2016.12.055

evidence_span

{"source_cache": "artifacts/acetate-research/2106256.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fc8e7ceab96e74e4664a17fce6b32ff0b498204a2c2c0df7437a4f6bfe1c5105", "start_char": 0, "end_char": 1005, "text_sha256": "fc8e7ceab96e74e4664a17fce6b32ff0b498204a2c2c0df7437a4f6bfe1c5105"}

experimental_model

Carbon-labelled acetate infusion in four to six human volunteers and in anaesthetised dogs

exposure

Infusion of acetate labelled at carbon 1 or carbon 2, with recovery measured as labelled carbon dioxide

limitations

A methodological result. It applies to every tracer study of substrate oxidation in this collection and elsewhere, and it means such studies underestimate oxidation unless corrected.

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 dog

plain_language

Where the label sits on the molecule changes how much comes back out as carbon dioxide, so tracer studies of acetate need correcting.

primary_references

[acetate-p2106256] Recovery of labeled CO2 during the infusion of C-1- vs C-2-labeled acetate: implications for tracer studies of substrate oxidation. (1990). https://pubmed.ncbi.nlm.nih.gov/2106256/ DOI: 10.1093/ajcn/51.2.248

tissue_or_cell_type

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 511–522

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Carbon-labelled acetate infusion in four to six human volunteers and in anaesthetised dogs · source_derived_draft · unverified_draft

### acetate-label-position-matters In postabsorptive volunteers 81.2% of infused label was recovered as labelled carbon dioxide from carbon-1 labelled acetate against 53.1% from carbon-2 labelled acetate, and in dogs recovery was 75.9% against 40.8%, leading to the conclusion that the position of the label in acetyl-CoA determines the extent to which oxidation of labelled acetyl-CoA is reflected in labelled carbon dioxide excretion. 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: Where the label sits on the molecule changes how much comes back out as carbon dioxide, so tracer studies of acetate need correcting. organism: Human and dog tissue_or_cell_type: Whole body experimental_model: Carbon-labelled acetate infusion in four to six human volunteers and in anaesthetised dogs limitations: A methodological result. It applies to every tracer study of substrate oxidation in this collection and elsewhere, and it means such studies underestimate oxidation unless corrected. exposure: Infusion of acetate labelled at carbon 1 or carbon 2, with recovery measured as labelled carbon dioxide evidence_span: {"source_cache": "artifacts/acetate-research/2106256.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fc8e7ceab96e74e4664a17fce6b32ff0b498204a2c2c0df7437a4f6bfe1c5105", "start_char": 0, "end_char": 1005, "text_sha256": "fc8e7ceab96e74e4664a17fce6b32ff0b498204a2c2c0df7437a4f6bfe1c5105"} [acetate-p2106256] Recovery of labeled CO2 during the infusion of C-1- vs C-2-labeled acetate: implications for tracer studies of substrate oxidation. (1990). https://pubmed.ncbi.nlm.nih.gov/2106256/ DOI: 10.1093/ajcn/51.2.248

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/acetate-research/32214246.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "302837a9fc88030dce2c74e65053f8baae65863245d2d811ccbb3231b95a99e1", "start_char": 0, "end_char": 1782, "text_sha256": "302837a9fc88030dce2c74e65053f8baae65863245d2d811ccbb3231b95a99e1"}

experimental_model

In vivo isotope tracing in mice with liver-specific Acly deletion, microbiota depletion and hepatic ACSS2 silencing

exposure

Bolus or gradual dietary fructose, with genetic, microbial and dose-rate manipulation

limitations

Three independent manipulations converge on the same route. Its dominance depends on how fast the fructose is eaten, and the human contribution is not established here.

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 sugar becomes acetate in the gut, and the liver builds fat out of that.

primary_references

[acetate-p32214246] Dietary fructose feeds hepatic lipogenesis via microbiota-derived acetate. (2020). https://pubmed.ncbi.nlm.nih.gov/32214246/ DOI: 10.1038/s41586-020-2101-7

tissue_or_cell_type

Liver and gut

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 563–574

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In vivo isotope tracing in mice with liver-specific Acly deletion, microbiota depletion and hepatic ACSS2 silencing · source_derived_draft · unverified_draft

### acetate-microbial-acetate-route Dietary fructose is converted to acetate by the gut microbiota and this supplies lipogenic acetyl-CoA independently of ACLY, with depletion of the microbiota or silencing of hepatic ACSS2, which generates acetyl-CoA from acetate, potently suppressing the conversion of bolus fructose into hepatic acetyl-CoA and fatty acids. 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 sugar becomes acetate in the gut, and the liver builds fat out of that. organism: Mouse tissue_or_cell_type: Liver and gut experimental_model: In vivo isotope tracing in mice with liver-specific Acly deletion, microbiota depletion and hepatic ACSS2 silencing limitations: Three independent manipulations converge on the same route. Its dominance depends on how fast the fructose is eaten, and the human contribution is not established here. exposure: Bolus or gradual dietary fructose, with genetic, microbial and dose-rate manipulation evidence_span: {"source_cache": "artifacts/acetate-research/32214246.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "302837a9fc88030dce2c74e65053f8baae65863245d2d811ccbb3231b95a99e1", "start_char": 0, "end_char": 1782, "text_sha256": "302837a9fc88030dce2c74e65053f8baae65863245d2d811ccbb3231b95a99e1"} [acetate-p32214246] Dietary fructose feeds hepatic lipogenesis via microbiota-derived acetate. (2020). https://pubmed.ncbi.nlm.nih.gov/32214246/ DOI: 10.1038/s41586-020-2101-7

evidence_span

{"source_cache": "artifacts/acetate-research/28099844.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6df5e8ccde04ad8a222db774f6a8b1e8838ad6a1d918ff84b667d6dde57de188", "start_char": 0, "end_char": 1134, "text_sha256": "6df5e8ccde04ad8a222db774f6a8b1e8838ad6a1d918ff84b667d6dde57de188"}

experimental_model

Quantitative analysis of acetate metabolism in cultured cells under oxygen and serum limitation

exposure

Exogenous acetate with ACSS2 and ACSS1 manipulation under oxygen and serum limitation

limitations

The quantitative accounting here is the important part and it is a limiting result: demand for two-carbon units far exceeds what exogenous acetate supplies. Cultured cells at a given acetate concentration, which is not a fed human.

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

Cultured cells

plain_language

An enzyme sitting on the chromatin catches the acetate released when marks are removed, and puts it straight back.

primary_references

[acetate-p28099844] Acetate Recapturing by Nuclear Acetyl-CoA Synthetase 2 Prevents Loss of Histone Acetylation during Oxygen and Serum Limitation. (2017). https://pubmed.ncbi.nlm.nih.gov/28099844/ DOI: 10.1016/j.celrep.2016.12.055

tissue_or_cell_type

Nucleus and cytosol

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 602–613

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Quantitative analysis of acetate metabolism in cultured cells under oxygen and serum limitation · source_derived_draft · unverified_draft

### acetate-nuclear-acss2-recapture Oxygen and serum limitation increased nuclear localisation of ACSS2, and nuclear ACSS2 recaptures acetate released from histone deacetylation for recycling by histone acetyltransferases, providing evidence for limited equilibration between nuclear and cytosolic acetyl-CoA and demonstrating that ACSS2 retains acetate to maintain histone acetylation. 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: An enzyme sitting on the chromatin catches the acetate released when marks are removed, and puts it straight back. organism: Cultured cells tissue_or_cell_type: Nucleus and cytosol experimental_model: Quantitative analysis of acetate metabolism in cultured cells under oxygen and serum limitation limitations: The quantitative accounting here is the important part and it is a limiting result: demand for two-carbon units far exceeds what exogenous acetate supplies. Cultured cells at a given acetate concentration, which is not a fed human. exposure: Exogenous acetate with ACSS2 and ACSS1 manipulation under oxygen and serum limitation evidence_span: {"source_cache": "artifacts/acetate-research/28099844.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6df5e8ccde04ad8a222db774f6a8b1e8838ad6a1d918ff84b667d6dde57de188", "start_char": 0, "end_char": 1134, "text_sha256": "6df5e8ccde04ad8a222db774f6a8b1e8838ad6a1d918ff84b667d6dde57de188"} [acetate-p28099844] Acetate Recapturing by Nuclear Acetyl-CoA Synthetase 2 Prevents Loss of Histone Acetylation during Oxygen and Serum Limitation. (2017). https://pubmed.ncbi.nlm.nih.gov/28099844/ DOI: 10.1016/j.celrep.2016.12.055

availability_state

machinery_impairment Imported condition classification; unverified.

dose

Bolus 2 g/kg labeled fructose plus 2 g/kg glucose; interventions specified by claim

duration

Acute isotope sampling up to 6 h

evidence_access

Primary full-text methods/results and metadata inspected.

evidence_scope

literature_reviewed; source-specific curation

experimental_model

Wild-type mice, microbiota depletion and liver Acss2-silencing experiments

exposure_scope

Component mixture

limitations

Carbon tracing supports microbial acetate supply; antibiotic depletion is not a clinical recommendation and microbiota effects are not universal across diets.

nutrient_topic

HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS

organism

Wild-type mice, microbiota depletion and liver Acss2-silencing experiments

plain_language

Silencing hepatic Acss2 suppressed conversion of bolus fructose carbon into hepatic acetyl-CoA and fatty acids in mice.

primary_references

Dietary fructose feeds hepatic lipogenesis via microbiota-derived acetate. (2020). https://pubmed.ncbi.nlm.nih.gov/32214246/ DOI: 10.1038/s41586-020-2101-7

route

Oral gavage and experimental microbiota/gene perturbation

tissue

Portal acetate and hepatic fatty-acid labeling

trigger_kind

machinery_impairment Imported condition classification; unverified.

High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 221–231

Original AI-assisted curation of twenty primary studies and official FDA composition information, with one reused canonical glucose-transport claim. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Wild-type mice, microbiota depletion and liver Acss2-silencing experiments · source_derived_draft · unverified_draft

## hfcs-acss2-silencing Silencing hepatic Acss2 suppressed conversion of bolus fructose carbon into hepatic acetyl-CoA and fatty acids in mice. Model/species: Wild-type mice, microbiota depletion and liver Acss2-silencing experiments Tissue: Portal acetate and hepatic fatty-acid labeling Exposure: Bolus 2 g/kg labeled fructose plus 2 g/kg glucose; interventions specified by claim Route: Oral gavage and experimental microbiota/gene perturbation Duration: Acute isotope sampling up to 6 h Exposure scope: Component mixture Limits: Carbon tracing supports microbial acetate supply; antibiotic depletion is not a clinical recommendation and microbiota effects are not universal across diets. Reference: Dietary fructose feeds hepatic lipogenesis via microbiota-derived acetate. (2020). https://pubmed.ncbi.nlm.nih.gov/32214246/ DOI: 10.1038/s41586-020-2101-7 Access: Primary full-text methods/results and metadata inspected.

evidence_span

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experimental_model

Anaerobic human fecal incubations before and after carbohydrate pre-feeding

exposure

Pectin and comparator carbohydrates; 48-hour incubations, up to two weeks of pre-feeding

limitations

Cultures lack intestinal absorption and host metabolism; results do not quantify systemic exposure.

nutrient_topic

Pectin research collection; topical membership is not evidence of a direct dietary effect. · Pectin, structurally heterogeneous plant polysaccharides

organism

Human fecal microbiota ex vivo

plain_language

Previous exposure changed the measured nitrogen-metabolism response.

primary_references

[pectin-p2317475] The effect of lactulose, pectin, arabinogalactan and cellulose on the production of organic acids and metabolism of ammonia by intestinal bacteria in a faecal incubation system. (1990). https://pubmed.ncbi.nlm.nih.gov/2317475/ DOI: 10.1079/bjn19900088

tissue_or_cell_type

Batch cultures

Pectin: metabolism, signaling and nutrient connections (2026-09-17) · lines 880–891

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Anaerobic human fecal incubations before and after carbohydrate pre-feeding · source_derived_draft · unverified_draft

### pectin-ammonia Pectin significantly reduced net ammonia generation in incubations after subjects had been pre-fed pectin; the reduction without pre-feeding was not significant. Condition category: normal nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Previous exposure changed the measured nitrogen-metabolism response. organism: Human fecal microbiota ex vivo tissue_or_cell_type: Batch cultures experimental_model: Anaerobic human fecal incubations before and after carbohydrate pre-feeding limitations: Cultures lack intestinal absorption and host metabolism; results do not quantify systemic exposure. exposure: Pectin and comparator carbohydrates; 48-hour incubations, up to two weeks of pre-feeding evidence_span: {"source_cache": "artifacts/pectin-research/2317475.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "86aae760cc52aeca6f270420e20dabaffa8167770fa30c7fa8e35b1f67b7d9b4", "start_char": 0, "end_char": 1642, "text_sha256": "86aae760cc52aeca6f270420e20dabaffa8167770fa30c7fa8e35b1f67b7d9b4"} [pectin-p2317475] The effect of lactulose, pectin, arabinogalactan and cellulose on the production of organic acids and metabolism of ammonia by intestinal bacteria in a faecal incubation system. (1990). https://pubmed.ncbi.nlm.nih.gov/2317475/ DOI: 10.1079/bjn19900088

evidence_span

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experimental_model

Human oral substrate challenge with blood SCFA measurements

exposure

20 g pectin after a 16-hour fast

limitations

Blood acetate is a systemic appearance measure, not a complete measure of colonic production or benefit.

nutrient_topic

Pectin research collection; topical membership is not evidence of a direct dietary effect. · Pectin, structurally heterogeneous plant polysaccharides

organism

Homo sapiens

plain_language

Microbial products can appear in blood hours after eating pectin.

primary_references

[pectin-p3998144] Carbohydrate fermentation in the human colon and its relation to acetate concentrations in venous blood. (1985). https://pubmed.ncbi.nlm.nih.gov/3998144/ DOI: 10.1172/jci111847

tissue_or_cell_type

Venous blood

Pectin: metabolism, signaling and nutrient connections (2026-09-17) · lines 893–904

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human oral substrate challenge with blood SCFA measurements · source_derived_draft · unverified_draft

### pectin-blood-acetate Blood acetate began rising about six hours after pectin and remained around twice fasting levels for the following 18 hours. Condition category: normal nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Microbial products can appear in blood hours after eating pectin. organism: Homo sapiens tissue_or_cell_type: Venous blood experimental_model: Human oral substrate challenge with blood SCFA measurements limitations: Blood acetate is a systemic appearance measure, not a complete measure of colonic production or benefit. exposure: 20 g pectin after a 16-hour fast evidence_span: {"source_cache": "artifacts/pectin-research/3998144.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "027517b7db8dce720509f94d183d6ab4b9bb6aed84e6ace679e421a72c31c6a6", "start_char": 0, "end_char": 1849, "text_sha256": "027517b7db8dce720509f94d183d6ab4b9bb6aed84e6ace679e421a72c31c6a6"} [pectin-p3998144] Carbohydrate fermentation in the human colon and its relation to acetate concentrations in venous blood. (1985). https://pubmed.ncbi.nlm.nih.gov/3998144/ DOI: 10.1172/jci111847

evidence_span

{"source_cache": "artifacts/pectin-research/2317475.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "86aae760cc52aeca6f270420e20dabaffa8167770fa30c7fa8e35b1f67b7d9b4", "start_char": 0, "end_char": 1642, "text_sha256": "86aae760cc52aeca6f270420e20dabaffa8167770fa30c7fa8e35b1f67b7d9b4"}

experimental_model

Anaerobic human fecal incubations before and after carbohydrate pre-feeding

exposure

Pectin and comparator carbohydrates; 48-hour incubations, up to two weeks of pre-feeding

limitations

Cultures lack intestinal absorption and host metabolism; results do not quantify systemic exposure.

nutrient_topic

Pectin research collection; topical membership is not evidence of a direct dietary effect. · Pectin, structurally heterogeneous plant polysaccharides

organism

Human fecal microbiota ex vivo

plain_language

Gut microbes can turn pectin into small organic acids.

primary_references

[pectin-p2317475] The effect of lactulose, pectin, arabinogalactan and cellulose on the production of organic acids and metabolism of ammonia by intestinal bacteria in a faecal incubation system. (1990). https://pubmed.ncbi.nlm.nih.gov/2317475/ DOI: 10.1079/bjn19900088

tissue_or_cell_type

Batch cultures

Pectin: metabolism, signaling and nutrient connections (2026-09-17) · lines 867–878

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Anaerobic human fecal incubations before and after carbohydrate pre-feeding · source_derived_draft · unverified_draft

### pectin-fermentation-scfa Added pectin increased SCFA generation in human fecal incubations; acetate was the major measured SCFA. Condition category: normal nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Gut microbes can turn pectin into small organic acids. organism: Human fecal microbiota ex vivo tissue_or_cell_type: Batch cultures experimental_model: Anaerobic human fecal incubations before and after carbohydrate pre-feeding limitations: Cultures lack intestinal absorption and host metabolism; results do not quantify systemic exposure. exposure: Pectin and comparator carbohydrates; 48-hour incubations, up to two weeks of pre-feeding evidence_span: {"source_cache": "artifacts/pectin-research/2317475.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "86aae760cc52aeca6f270420e20dabaffa8167770fa30c7fa8e35b1f67b7d9b4", "start_char": 0, "end_char": 1642, "text_sha256": "86aae760cc52aeca6f270420e20dabaffa8167770fa30c7fa8e35b1f67b7d9b4"} [pectin-p2317475] The effect of lactulose, pectin, arabinogalactan and cellulose on the production of organic acids and metabolism of ammonia by intestinal bacteria in a faecal incubation system. (1990). https://pubmed.ncbi.nlm.nih.gov/2317475/ DOI: 10.1079/bjn19900088