Nutrient chapter

Acetic acid

Acetic acid, the ingested dietary acid, as supplied by vinegar. This entity is the exposure that is swallowed and is deliberately distinct from acetate, the circulating anion, which in this ledger also arrives from gut fermentation of fibre, from gut fermentation of fructose, and from hepatic alcohol metabolism. The two are not linked as a family; the step from ingestion to plasma acetate is recorded as its own claim. Species, exposure and limitations are retained in each linked claim.

51 recorded mechanisms · 3 availability situations · 1 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

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.
Acetic acid → Acetate source_derived_draftungraded
Experimental context and source evidence
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/
Complete structured claim and evidence
The glucose response was depressed by 31.4% after the acetic acid plus bread meal with respect to the sodium acetate plus bread meal and the blank plus bread meal, and the authors concluded that a limited dose of vinegar as salad dressing significantly influences the glycaemic response by a mechanism related to acidity but not to gastric emptying.
Native vinegar supplying free acetic acid → Postprandial blood glucose response source_derived_draftungraded
Experimental context and source evidence
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"}
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
The acid form lowered blood glucose by about a third; the neutralised form did not.
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 82–93
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-acid-lowers-glucose The glucose response was depressed by 31.4% after the acetic acid plus bread meal with respect to the sodium acetate plus bread meal and the blank plus bread meal, and the authors concluded that a limited dose of vinegar as salad dressing significantly influences the glycaemic response by a mechanism related to acidity but not to gastric emptying. 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 acid form lowered blood glucose by about a third; the neutralised form did not. 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/
Complete structured claim and evidence
No difference was observed between gastric emptying times after the acetic acid plus bread meal and the sodium acetate plus bread meal, measured by ultrasonography in four subjects.
Native vinegar supplying free acetic acid → Gastric emptying rate measured as the change in antral cross-sectional area by real-time ultrasonography source_derived_draftungraded
Experimental context and source evidence
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"}
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
The two forms emptied the stomach at the same rate, while only one lowered glucose.
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 95–106
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-emptying-not-different No difference was observed between gastric emptying times after the acetic acid plus bread meal and the sodium acetate plus bread meal, measured by ultrasonography in four subjects. 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 two forms emptied the stomach at the same rate, while only one lowered glucose. 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/
Complete structured claim and evidence
The presence of acetic acid given as vinegar significantly reduced the postprandial glucose and insulin responses to a starchy meal, with a glycaemic index of 64 and an insulinaemic index of 65 against the white bread reference meal.
Acetic acid → Postprandial blood glucose response source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/9630389.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "03f693ed6a9ae1c12e1d9cdb83a2d6001d8b128458092ca61ae33033da8af780", "start_char": 0, "end_char": 1289, "text_sha256": "03f693ed6a9ae1c12e1d9cdb83a2d6001d8b128458092ca61ae33033da8af780"}
experimental_model
Randomised crossover in ten healthy volunteers aged 22 to 51, with paracetamol as an emptying marker
exposure
Vinegar added to a white bread reference meal matched for starch, protein and fat
limitations
Paracetamol appearance is an indirect marker of emptying. The authors state the mechanism is probably delayed emptying, which the neutralised-vinegar study in this collection argues against.
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
Vinegar with a starchy meal cut both the glucose and the insulin rise by about a third.
primary_references
[acetate-p9630389] Delayed gastric emptying rate may explain improved glycaemia in healthy subjects to a starchy meal with added vinegar. (1998). https://pubmed.ncbi.nlm.nih.gov/9630389/ DOI: 10.1038/sj.ejcn.1600572
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 108–119
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised crossover in ten healthy volunteers aged 22 to 51, with paracetamol as an emptying marker · source_derived_draft · unverified_draft
### acetate-vinegar-glycaemia The presence of acetic acid given as vinegar significantly reduced the postprandial glucose and insulin responses to a starchy meal, with a glycaemic index of 64 and an insulinaemic index of 65 against the white bread reference meal. 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: Vinegar with a starchy meal cut both the glucose and the insulin rise by about a third. organism: Human tissue_or_cell_type: Whole body and stomach experimental_model: Randomised crossover in ten healthy volunteers aged 22 to 51, with paracetamol as an emptying marker limitations: Paracetamol appearance is an indirect marker of emptying. The authors state the mechanism is probably delayed emptying, which the neutralised-vinegar study in this collection argues against. exposure: Vinegar added to a white bread reference meal matched for starch, protein and fat evidence_span: {"source_cache": "artifacts/acetate-research/9630389.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "03f693ed6a9ae1c12e1d9cdb83a2d6001d8b128458092ca61ae33033da8af780", "start_char": 0, "end_char": 1289, "text_sha256": "03f693ed6a9ae1c12e1d9cdb83a2d6001d8b128458092ca61ae33033da8af780"} [acetate-p9630389] Delayed gastric emptying rate may explain improved glycaemia in healthy subjects to a starchy meal with added vinegar. (1998). https://pubmed.ncbi.nlm.nih.gov/9630389/ DOI: 10.1038/sj.ejcn.1600572
Complete structured claim and evidence
As judged from lowered paracetamol levels after the test meal with vinegar, the authors concluded that the mechanism is probably a delayed gastric emptying rate.
Acetic acid → Paracetamol appearance as a marker of gastric emptying rate source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/9630389.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "03f693ed6a9ae1c12e1d9cdb83a2d6001d8b128458092ca61ae33033da8af780", "start_char": 0, "end_char": 1289, "text_sha256": "03f693ed6a9ae1c12e1d9cdb83a2d6001d8b128458092ca61ae33033da8af780"}
experimental_model
Randomised crossover in ten healthy volunteers aged 22 to 51, with paracetamol as an emptying marker
exposure
Vinegar added to a white bread reference meal matched for starch, protein and fat
limitations
Paracetamol appearance is an indirect marker of emptying. The authors state the mechanism is probably delayed emptying, which the neutralised-vinegar study in this collection argues against.
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
A marker drug appeared more slowly, which was read as the stomach emptying more slowly.
primary_references
[acetate-p9630389] Delayed gastric emptying rate may explain improved glycaemia in healthy subjects to a starchy meal with added vinegar. (1998). https://pubmed.ncbi.nlm.nih.gov/9630389/ DOI: 10.1038/sj.ejcn.1600572
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 121–132
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised crossover in ten healthy volunteers aged 22 to 51, with paracetamol as an emptying marker · source_derived_draft · unverified_draft
### acetate-emptying-explanation As judged from lowered paracetamol levels after the test meal with vinegar, the authors concluded that the mechanism is probably a delayed gastric emptying rate. 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 marker drug appeared more slowly, which was read as the stomach emptying more slowly. organism: Human tissue_or_cell_type: Whole body and stomach experimental_model: Randomised crossover in ten healthy volunteers aged 22 to 51, with paracetamol as an emptying marker limitations: Paracetamol appearance is an indirect marker of emptying. The authors state the mechanism is probably delayed emptying, which the neutralised-vinegar study in this collection argues against. exposure: Vinegar added to a white bread reference meal matched for starch, protein and fat evidence_span: {"source_cache": "artifacts/acetate-research/9630389.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "03f693ed6a9ae1c12e1d9cdb83a2d6001d8b128458092ca61ae33033da8af780", "start_char": 0, "end_char": 1289, "text_sha256": "03f693ed6a9ae1c12e1d9cdb83a2d6001d8b128458092ca61ae33033da8af780"} [acetate-p9630389] Delayed gastric emptying rate may explain improved glycaemia in healthy subjects to a starchy meal with added vinegar. (1998). https://pubmed.ncbi.nlm.nih.gov/9630389/ DOI: 10.1038/sj.ejcn.1600572
Complete structured claim and evidence
A significant dose-response relation was seen at 30 minutes for blood glucose and serum insulin, the higher the acetic acid level the lower the metabolic responses, though the glycaemic and insulinaemic index lowering was significant when calculated on the 90 minute incremental area and the corresponding 120 minute values did not differ from the reference meal.
Acetic acid → Postprandial blood glucose response source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/16015276.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6ab7baf7d6544a409fc34e34b0a51ba924332938e1467dbbf8323789c3f7d6d3", "start_char": 0, "end_char": 2189, "text_sha256": "6ab7baf7d6544a409fc34e34b0a51ba924332938e1467dbbf8323789c3f7d6d3"}
experimental_model
Randomised crossover in twelve healthy volunteers with three graded vinegar doses
exposure
Vinegar supplying 18, 23 or 28 mmol acetic acid with white wheat bread containing 50 g available carbohydrate
limitations
A dose-response design. The glycaemic and insulinaemic index lowering was significant on the 90 minute incremental area but not on the 120 minute area, so the effect is on the early part of the curve.
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
More acid meant a smaller glucose and insulin rise, and the effect is on the first hour and a half rather than the whole curve.
primary_references
[acetate-p16015276] Vinegar supplementation lowers glucose and insulin responses and increases satiety after a bread meal in healthy subjects. (2005). https://pubmed.ncbi.nlm.nih.gov/16015276/ DOI: 10.1038/sj.ejcn.1602197
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 134–145
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised crossover in twelve healthy volunteers with three graded vinegar doses · source_derived_draft · unverified_draft
### acetate-vinegar-dose-response A significant dose-response relation was seen at 30 minutes for blood glucose and serum insulin, the higher the acetic acid level the lower the metabolic responses, though the glycaemic and insulinaemic index lowering was significant when calculated on the 90 minute incremental area and the corresponding 120 minute values did not differ from the reference meal. 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: More acid meant a smaller glucose and insulin rise, and the effect is on the first hour and a half rather than the whole curve. organism: Human tissue_or_cell_type: Whole body experimental_model: Randomised crossover in twelve healthy volunteers with three graded vinegar doses limitations: A dose-response design. The glycaemic and insulinaemic index lowering was significant on the 90 minute incremental area but not on the 120 minute area, so the effect is on the early part of the curve. exposure: Vinegar supplying 18, 23 or 28 mmol acetic acid with white wheat bread containing 50 g available carbohydrate evidence_span: {"source_cache": "artifacts/acetate-research/16015276.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6ab7baf7d6544a409fc34e34b0a51ba924332938e1467dbbf8323789c3f7d6d3", "start_char": 0, "end_char": 2189, "text_sha256": "6ab7baf7d6544a409fc34e34b0a51ba924332938e1467dbbf8323789c3f7d6d3"} [acetate-p16015276] Vinegar supplementation lowers glucose and insulin responses and increases satiety after a bread meal in healthy subjects. (2005). https://pubmed.ncbi.nlm.nih.gov/16015276/ DOI: 10.1038/sj.ejcn.1602197
Complete structured claim and evidence
The rating of satiety was directly related to the acetic acid level, with a linear dose-response relation, and the highest level of vinegar increased the satiety score at 30, 90 and 120 minutes after the meal.
Acetic acid → Subjective satiety rating after a meal source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/16015276.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6ab7baf7d6544a409fc34e34b0a51ba924332938e1467dbbf8323789c3f7d6d3", "start_char": 0, "end_char": 2189, "text_sha256": "6ab7baf7d6544a409fc34e34b0a51ba924332938e1467dbbf8323789c3f7d6d3"}
experimental_model
Randomised crossover in twelve healthy volunteers with three graded vinegar doses
exposure
Vinegar supplying 18, 23 or 28 mmol acetic acid with white wheat bread containing 50 g available carbohydrate
limitations
A dose-response design. The glycaemic and insulinaemic index lowering was significant on the 90 minute incremental area but not on the 120 minute area, so the effect is on the early part of the curve.
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
The more acid, the fuller people said they felt, and the feeling lasted two hours.
primary_references
[acetate-p16015276] Vinegar supplementation lowers glucose and insulin responses and increases satiety after a bread meal in healthy subjects. (2005). https://pubmed.ncbi.nlm.nih.gov/16015276/ DOI: 10.1038/sj.ejcn.1602197
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 147–158
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised crossover in twelve healthy volunteers with three graded vinegar doses · source_derived_draft · unverified_draft
### acetate-vinegar-satiety The rating of satiety was directly related to the acetic acid level, with a linear dose-response relation, and the highest level of vinegar increased the satiety score at 30, 90 and 120 minutes after the meal. 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 more acid, the fuller people said they felt, and the feeling lasted two hours. organism: Human tissue_or_cell_type: Whole body experimental_model: Randomised crossover in twelve healthy volunteers with three graded vinegar doses limitations: A dose-response design. The glycaemic and insulinaemic index lowering was significant on the 90 minute incremental area but not on the 120 minute area, so the effect is on the early part of the curve. exposure: Vinegar supplying 18, 23 or 28 mmol acetic acid with white wheat bread containing 50 g available carbohydrate evidence_span: {"source_cache": "artifacts/acetate-research/16015276.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6ab7baf7d6544a409fc34e34b0a51ba924332938e1467dbbf8323789c3f7d6d3", "start_char": 0, "end_char": 2189, "text_sha256": "6ab7baf7d6544a409fc34e34b0a51ba924332938e1467dbbf8323789c3f7d6d3"} [acetate-p16015276] Vinegar supplementation lowers glucose and insulin responses and increases satiety after a bread meal in healthy subjects. (2005). https://pubmed.ncbi.nlm.nih.gov/16015276/ DOI: 10.1038/sj.ejcn.1602197
Complete structured claim and evidence
The glycaemic and insulinaemic indices of cold potatoes with added vinegar were significantly reduced by 43% and 31% respectively compared with freshly boiled potatoes; vinegar was tested only together with cold storage in this design.
Acetic acid → Postprandial blood glucose response source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/16034360.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "46b8b5f47f2fcecc5fd70b32aca316fe7065dc407147d4f7b2c63bdf8f486f5c", "start_char": 0, "end_char": 1811, "text_sha256": "46b8b5f47f2fcecc5fd70b32aca316fe7065dc407147d4f7b2c63bdf8f486f5c"}
experimental_model
Four-meal randomised crossover in thirteen healthy subjects
exposure
Freshly boiled potato, cold-stored potato, cold-stored potato with a vinaigrette of 8 g olive oil and 28 g of 6% white vinegar, against a white bread reference
limitations
Vinegar was tested only in combination with cold storage, so this design cannot separate the two. Cold storage alone was tested and is recorded separately.
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
Cold potato dressed in vinegar produced a much smaller glucose and insulin rise than hot potato, but the two changes were not separated.
primary_references
[acetate-p16034360] Vinegar dressing and cold storage of potatoes lowers postprandial glycaemic and insulinaemic responses in healthy subjects. (2005). https://pubmed.ncbi.nlm.nih.gov/16034360/ DOI: 10.1038/sj.ejcn.1602238
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 160–171
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-meal randomised crossover in thirteen healthy subjects · source_derived_draft · unverified_draft
### acetate-cold-plus-vinegar The glycaemic and insulinaemic indices of cold potatoes with added vinegar were significantly reduced by 43% and 31% respectively compared with freshly boiled potatoes; vinegar was tested only together with cold storage in this design. 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: Cold potato dressed in vinegar produced a much smaller glucose and insulin rise than hot potato, but the two changes were not separated. organism: Human tissue_or_cell_type: Whole body experimental_model: Four-meal randomised crossover in thirteen healthy subjects limitations: Vinegar was tested only in combination with cold storage, so this design cannot separate the two. Cold storage alone was tested and is recorded separately. exposure: Freshly boiled potato, cold-stored potato, cold-stored potato with a vinaigrette of 8 g olive oil and 28 g of 6% white vinegar, against a white bread reference evidence_span: {"source_cache": "artifacts/acetate-research/16034360.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "46b8b5f47f2fcecc5fd70b32aca316fe7065dc407147d4f7b2c63bdf8f486f5c", "start_char": 0, "end_char": 1811, "text_sha256": "46b8b5f47f2fcecc5fd70b32aca316fe7065dc407147d4f7b2c63bdf8f486f5c"} [acetate-p16034360] Vinegar dressing and cold storage of potatoes lowers postprandial glycaemic and insulinaemic responses in healthy subjects. (2005). https://pubmed.ncbi.nlm.nih.gov/16034360/ DOI: 10.1038/sj.ejcn.1602238
Complete structured claim and evidence
Cold storage of boiled potatoes increased resistant starch content significantly from 3.3% to 5.2% on a starch basis, and cold storage on its own lowered the insulinaemic index by 28% compared with freshly boiled potatoes.
Boiled potato cold-stored at 8 degrees for 24 hours, raising resistant starch content → Postprandial insulin response source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/16034360.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "46b8b5f47f2fcecc5fd70b32aca316fe7065dc407147d4f7b2c63bdf8f486f5c", "start_char": 0, "end_char": 1811, "text_sha256": "46b8b5f47f2fcecc5fd70b32aca316fe7065dc407147d4f7b2c63bdf8f486f5c"}
experimental_model
Four-meal randomised crossover in thirteen healthy subjects
exposure
Freshly boiled potato, cold-stored potato, cold-stored potato with a vinaigrette of 8 g olive oil and 28 g of 6% white vinegar, against a white bread reference
limitations
Vinegar was tested only in combination with cold storage, so this design cannot separate the two. Cold storage alone was tested and is recorded separately.
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
Cooling the potato alone raised its resistant starch and cut the insulin response by a quarter.
primary_references
[acetate-p16034360] Vinegar dressing and cold storage of potatoes lowers postprandial glycaemic and insulinaemic responses in healthy subjects. (2005). https://pubmed.ncbi.nlm.nih.gov/16034360/ DOI: 10.1038/sj.ejcn.1602238
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 173–184
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-meal randomised crossover in thirteen healthy subjects · source_derived_draft · unverified_draft
### acetate-cold-storage-alone Cold storage of boiled potatoes increased resistant starch content significantly from 3.3% to 5.2% on a starch basis, and cold storage on its own lowered the insulinaemic index by 28% compared with freshly boiled potatoes. 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: Cooling the potato alone raised its resistant starch and cut the insulin response by a quarter. organism: Human tissue_or_cell_type: Whole body experimental_model: Four-meal randomised crossover in thirteen healthy subjects limitations: Vinegar was tested only in combination with cold storage, so this design cannot separate the two. Cold storage alone was tested and is recorded separately. exposure: Freshly boiled potato, cold-stored potato, cold-stored potato with a vinaigrette of 8 g olive oil and 28 g of 6% white vinegar, against a white bread reference evidence_span: {"source_cache": "artifacts/acetate-research/16034360.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "46b8b5f47f2fcecc5fd70b32aca316fe7065dc407147d4f7b2c63bdf8f486f5c", "start_char": 0, "end_char": 1811, "text_sha256": "46b8b5f47f2fcecc5fd70b32aca316fe7065dc407147d4f7b2c63bdf8f486f5c"} [acetate-p16034360] Vinegar dressing and cold storage of potatoes lowers postprandial glycaemic and insulinaemic responses in healthy subjects. (2005). https://pubmed.ncbi.nlm.nih.gov/16034360/ DOI: 10.1038/sj.ejcn.1602238
Complete structured claim and evidence
In patients with type 1 diabetes and diabetic gastroparesis the median gastric emptying rate was 27% without vinegar and 17% with vinegar, a statistically significant reduction, and the authors concluded this might be a disadvantage for their glycaemic control.
Apple cider vinegar as used in the type 1 diabetes trial → Gastric emptying rate measured as the change in antral cross-sectional area by real-time ultrasonography source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/acetate-research/18093343.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "092c8db0cd31e510e21838bd5ad6cc16876368af06584a2fc6d44efa2e189439", "start_char": 0, "end_char": 1477, "text_sha256": "092c8db0cd31e510e21838bd5ad6cc16876368af06584a2fc6d44efa2e189439"}
experimental_model
Investigator-blinded crossover in ten patients with type 1 diabetes and diabetic gastroparesis
exposure
30 ml apple cider vinegar in 200 ml water daily before breakfast for two weeks, with gastric emptying measured by standardised real-time ultrasonography after 300 g rice pudding
limitations
Ten patients, one of whom had undergone vagotomy. It is recorded because the same mechanism that is read as a benefit in healthy people is unwanted in people whose stomachs already empty too slowly.
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
In people whose stomachs already empty too slowly, vinegar made that worse.
primary_references
[acetate-p18093343] Effect of apple cider vinegar on delayed gastric emptying in patients with type 1 diabetes mellitus: a pilot study. (2007). https://pubmed.ncbi.nlm.nih.gov/18093343/ DOI: 10.1186/1471-230x-7-46
tissue_or_cell_type
Stomach
trigger_kind
biomarker_context 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 186–197
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Investigator-blinded crossover in ten patients with type 1 diabetes and diabetic gastroparesis · source_derived_draft · unverified_draft
### acetate-vinegar-worsens-gastroparesis In patients with type 1 diabetes and diabetic gastroparesis the median gastric emptying rate was 27% without vinegar and 17% with vinegar, a statistically significant reduction, and the authors concluded this might be a disadvantage for their glycaemic control. Condition category: biomarker_context 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 people whose stomachs already empty too slowly, vinegar made that worse. organism: Human tissue_or_cell_type: Stomach experimental_model: Investigator-blinded crossover in ten patients with type 1 diabetes and diabetic gastroparesis limitations: Ten patients, one of whom had undergone vagotomy. It is recorded because the same mechanism that is read as a benefit in healthy people is unwanted in people whose stomachs already empty too slowly. exposure: 30 ml apple cider vinegar in 200 ml water daily before breakfast for two weeks, with gastric emptying measured by standardised real-time ultrasonography after 300 g rice pudding evidence_span: {"source_cache": "artifacts/acetate-research/18093343.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "092c8db0cd31e510e21838bd5ad6cc16876368af06584a2fc6d44efa2e189439", "start_char": 0, "end_char": 1477, "text_sha256": "092c8db0cd31e510e21838bd5ad6cc16876368af06584a2fc6d44efa2e189439"} [acetate-p18093343] Effect of apple cider vinegar on delayed gastric emptying in patients with type 1 diabetes mellitus: a pilot study. (2007). https://pubmed.ncbi.nlm.nih.gov/18093343/ DOI: 10.1186/1471-230x-7-46
Complete structured claim and evidence
Body weight, body mass index, visceral fat area, waist circumference and serum triglyceride levels were significantly lower in both vinegar intake groups than in the placebo group after 12 weeks.
Acetic acid → Visceral fat area source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/19661687.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bcc0d712702f1a020d98a208a90656ef5429bcbfe87257559a6919d673459955", "start_char": 0, "end_char": 884, "text_sha256": "bcc0d712702f1a020d98a208a90656ef5429bcbfe87257559a6919d673459955"}
experimental_model
Double-blind randomised trial in obese Japanese subjects over 12 weeks
exposure
500 ml daily of a beverage containing 15 ml vinegar (750 mg acetic acid), 30 ml vinegar (1500 mg acetic acid), or no vinegar
limitations
The longest human exposure in this collection. A single population, and the measured endpoints are anthropometric rather than mechanistic.
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
Over twelve weeks, daily vinegar lowered weight, waist, visceral fat and blood triglycerides.
primary_references
[acetate-p19661687] Vinegar intake reduces body weight, body fat mass, and serum triglyceride levels in obese Japanese subjects. (2009). https://pubmed.ncbi.nlm.nih.gov/19661687/ DOI: 10.1271/bbb.90231
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 199–210
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomised trial in obese Japanese subjects over 12 weeks · source_derived_draft · unverified_draft
### acetate-vinegar-body-fat Body weight, body mass index, visceral fat area, waist circumference and serum triglyceride levels were significantly lower in both vinegar intake groups than in the placebo group after 12 weeks. 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: Over twelve weeks, daily vinegar lowered weight, waist, visceral fat and blood triglycerides. organism: Human tissue_or_cell_type: Whole body experimental_model: Double-blind randomised trial in obese Japanese subjects over 12 weeks limitations: The longest human exposure in this collection. A single population, and the measured endpoints are anthropometric rather than mechanistic. exposure: 500 ml daily of a beverage containing 15 ml vinegar (750 mg acetic acid), 30 ml vinegar (1500 mg acetic acid), or no vinegar evidence_span: {"source_cache": "artifacts/acetate-research/19661687.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bcc0d712702f1a020d98a208a90656ef5429bcbfe87257559a6919d673459955", "start_char": 0, "end_char": 884, "text_sha256": "bcc0d712702f1a020d98a208a90656ef5429bcbfe87257559a6919d673459955"} [acetate-p19661687] Vinegar intake reduces body weight, body fat mass, and serum triglyceride levels in obese Japanese subjects. (2009). https://pubmed.ncbi.nlm.nih.gov/19661687/ DOI: 10.1271/bbb.90231
Complete structured claim and evidence
A 39-year-old woman who drank one tablespoon of white vinegar to soften a crab shell stuck in her throat was found on endoscopy to have inflammation of the oropharynx and second-degree caustic injury of the oesophagus extending to the cardia, with an uneventful recovery.
Acetic acid → Caustic injury of the oropharynx and oesophagus source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/12376715.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "028d663eb0bf09494f45ded6c6045d6fc40a2ac3c0ae1a3a6dab5fafef985e55", "start_char": 0, "end_char": 482, "text_sha256": "028d663eb0bf09494f45ded6c6045d6fc40a2ac3c0ae1a3a6dab5fafef985e55"}
experimental_model
Single clinical case report with endoscopy
exposure
One tablespoon of white vinegar swallowed to dislodge a crab shell from the throat
limitations
A single case. It establishes that the same compound is corrosive at the concentration sold for cooking, which none of the dietary studies address.
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
One tablespoon, swallowed neat, burned the throat and the length of the gullet.
primary_references
[acetate-p12376715] Corrosive oesophageal injury following vinegar ingestion. (2002). https://pubmed.ncbi.nlm.nih.gov/12376715/
tissue_or_cell_type
Oropharynx and oesophagus
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 212–223
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single clinical case report with endoscopy · source_derived_draft · unverified_draft
### acetate-corrosive-injury A 39-year-old woman who drank one tablespoon of white vinegar to soften a crab shell stuck in her throat was found on endoscopy to have inflammation of the oropharynx and second-degree caustic injury of the oesophagus extending to the cardia, with an uneventful recovery. 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: One tablespoon, swallowed neat, burned the throat and the length of the gullet. organism: Human tissue_or_cell_type: Oropharynx and oesophagus experimental_model: Single clinical case report with endoscopy limitations: A single case. It establishes that the same compound is corrosive at the concentration sold for cooking, which none of the dietary studies address. exposure: One tablespoon of white vinegar swallowed to dislodge a crab shell from the throat evidence_span: {"source_cache": "artifacts/acetate-research/12376715.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "028d663eb0bf09494f45ded6c6045d6fc40a2ac3c0ae1a3a6dab5fafef985e55", "start_char": 0, "end_char": 482, "text_sha256": "028d663eb0bf09494f45ded6c6045d6fc40a2ac3c0ae1a3a6dab5fafef985e55"} [acetate-p12376715] Corrosive oesophageal injury following vinegar ingestion. (2002). https://pubmed.ncbi.nlm.nih.gov/12376715/
Complete structured claim and evidence
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.
Acetate → Human free fatty acid receptor 2 / FFAR2 source_derived_draftungraded
Experimental context and source evidence
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"}
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
Complete structured claim and evidence
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.
Human free fatty acid receptor 3 / FFAR3 → Acetate source_derived_draftungraded
Experimental context and source evidence
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"}
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
Complete structured claim and evidence
GPR43-deficient mice were obese on a normal diet whereas mice overexpressing GPR43 specifically in adipose tissue remained lean even when fed a high-fat diet, and raised under germ-free conditions or after treatment with antibiotics both types of mice had a normal phenotype.
Human free fatty acid receptor 2 / FFAR2 → Fat accumulation in adipose tissue source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/acetate-research/23652017.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "52bcd2cce838e217b7115f23092863912a2fad5dbece809485fa06c9c06d8d60", "start_char": 0, "end_char": 1122, "text_sha256": "52bcd2cce838e217b7115f23092863912a2fad5dbece809485fa06c9c06d8d60"}
experimental_model
GPR43-deficient and adipose-overexpressing mice, raised conventionally, germ-free and after antibiotics
exposure
Normal and high-fat diet, with germ-free rearing and antibiotic treatment as controls
limitations
The germ-free control is what ties the receptor phenotype to microbial short-chain fatty acids rather than to the receptor alone. The receptor senses all short-chain fatty acids, not acetate specifically.
nutrient_topic
Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
organism
Mouse
plain_language
The receptor keeps fat off, and only when gut bacteria are there to supply its signal.
primary_references
[acetate-p23652017] The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43. (2013). https://pubmed.ncbi.nlm.nih.gov/23652017/ DOI: 10.1038/ncomms2852
tissue_or_cell_type
Adipose tissue and whole body
trigger_kind
machinery_impairment Imported condition classification; unverified.
Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 251–262
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GPR43-deficient and adipose-overexpressing mice, raised conventionally, germ-free and after antibiotics · source_derived_draft · unverified_draft
### acetate-ffar2-suppresses-fat GPR43-deficient mice were obese on a normal diet whereas mice overexpressing GPR43 specifically in adipose tissue remained lean even when fed a high-fat diet, and raised under germ-free conditions or after treatment with antibiotics both types of mice had a normal phenotype. Condition category: machinery_impairment nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: The receptor keeps fat off, and only when gut bacteria are there to supply its signal. organism: Mouse tissue_or_cell_type: Adipose tissue and whole body experimental_model: GPR43-deficient and adipose-overexpressing mice, raised conventionally, germ-free and after antibiotics limitations: The germ-free control is what ties the receptor phenotype to microbial short-chain fatty acids rather than to the receptor alone. The receptor senses all short-chain fatty acids, not acetate specifically. exposure: Normal and high-fat diet, with germ-free rearing and antibiotic treatment as controls evidence_span: {"source_cache": "artifacts/acetate-research/23652017.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "52bcd2cce838e217b7115f23092863912a2fad5dbece809485fa06c9c06d8d60", "start_char": 0, "end_char": 1122, "text_sha256": "52bcd2cce838e217b7115f23092863912a2fad5dbece809485fa06c9c06d8d60"} [acetate-p23652017] The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43. (2013). https://pubmed.ncbi.nlm.nih.gov/23652017/ DOI: 10.1038/ncomms2852
Complete structured claim and evidence
Short-chain fatty acid-mediated activation of GPR43 suppressed insulin signalling in adipocytes, which inhibited fat accumulation in adipose tissue and promoted the metabolism of unincorporated lipids and glucose in other tissues, establishing GPR43 as a sensor for excessive dietary energy.
Human free fatty acid receptor 2 / FFAR2 → Insulin signalling in adipocytes source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
GPR43-deficient and adipose-overexpressing mice, raised conventionally, germ-free and after antibiotics
exposure
Normal and high-fat diet, with germ-free rearing and antibiotic treatment as controls
limitations
The germ-free control is what ties the receptor phenotype to microbial short-chain fatty acids rather than to the receptor alone. The receptor senses all short-chain fatty acids, not acetate specifically.
nutrient_topic
Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
organism
Mouse
plain_language
The signal tells fat cells to stop taking on more, and sends the fuel elsewhere.
primary_references
[acetate-p23652017] The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43. (2013). https://pubmed.ncbi.nlm.nih.gov/23652017/ DOI: 10.1038/ncomms2852
tissue_or_cell_type
Adipose tissue and whole body
Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 264–275
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GPR43-deficient and adipose-overexpressing mice, raised conventionally, germ-free and after antibiotics · source_derived_draft · unverified_draft
### acetate-ffar2-insulin-signalling Short-chain fatty acid-mediated activation of GPR43 suppressed insulin signalling in adipocytes, which inhibited fat accumulation in adipose tissue and promoted the metabolism of unincorporated lipids and glucose in other tissues, establishing GPR43 as a sensor for excessive dietary energy. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: The signal tells fat cells to stop taking on more, and sends the fuel elsewhere. organism: Mouse tissue_or_cell_type: Adipose tissue and whole body experimental_model: GPR43-deficient and adipose-overexpressing mice, raised conventionally, germ-free and after antibiotics limitations: The germ-free control is what ties the receptor phenotype to microbial short-chain fatty acids rather than to the receptor alone. The receptor senses all short-chain fatty acids, not acetate specifically. exposure: Normal and high-fat diet, with germ-free rearing and antibiotic treatment as controls evidence_span: {"source_cache": "artifacts/acetate-research/23652017.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "52bcd2cce838e217b7115f23092863912a2fad5dbece809485fa06c9c06d8d60", "start_char": 0, "end_char": 1122, "text_sha256": "52bcd2cce838e217b7115f23092863912a2fad5dbece809485fa06c9c06d8d60"} [acetate-p23652017] The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43. (2013). https://pubmed.ncbi.nlm.nih.gov/23652017/ DOI: 10.1038/ncomms2852
Complete structured claim and evidence
GPR43 immunoreactivity was localised to enteroendocrine cells expressing peptide YY, whereas 5-hydroxytryptamine-immunoreactive enteroendocrine cells were not immunoreactive for GPR43, and mast cells of the lamina propria expressing 5-hydroxytryptamine were also GPR43-immunoreactive.
Human free fatty acid receptor 2 / FFAR2 → Enteroendocrine cell source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/16453106.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14165574bceda6c6197de30baae79895b87d2b95272ea42c231554d7a4c015d2", "start_char": 0, "end_char": 1605, "text_sha256": "14165574bceda6c6197de30baae79895b87d2b95272ea42c231554d7a4c015d2"}
experimental_model
RT-PCR, Western blotting and immunohistochemistry with a rat-specific GPR43 antiserum
exposure
Receptor localisation across mucosal cell types
limitations
An anatomical result naming the cells that carry the receptor. Localisation is not function, and the antiserum was raised against a synthesised fragment.
nutrient_topic
Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
organism
Rat
plain_language
The receptor sits on the gut cells that make PYY, and on mast cells, but not on the serotonin-making gut cells.
primary_references
[acetate-p16453106] Short-chain fatty acid receptor, GPR43, is expressed by enteroendocrine cells and mucosal mast cells in rat intestine. (2006). https://pubmed.ncbi.nlm.nih.gov/16453106/ DOI: 10.1007/s00441-005-0140-x
tissue_or_cell_type
Distal ileum and colon
Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 277–288
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · RT-PCR, Western blotting and immunohistochemistry with a rat-specific GPR43 antiserum · source_derived_draft · unverified_draft
### acetate-ffar2-on-pyy-cells GPR43 immunoreactivity was localised to enteroendocrine cells expressing peptide YY, whereas 5-hydroxytryptamine-immunoreactive enteroendocrine cells were not immunoreactive for GPR43, and mast cells of the lamina propria expressing 5-hydroxytryptamine were also GPR43-immunoreactive. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: The receptor sits on the gut cells that make PYY, and on mast cells, but not on the serotonin-making gut cells. organism: Rat tissue_or_cell_type: Distal ileum and colon experimental_model: RT-PCR, Western blotting and immunohistochemistry with a rat-specific GPR43 antiserum limitations: An anatomical result naming the cells that carry the receptor. Localisation is not function, and the antiserum was raised against a synthesised fragment. exposure: Receptor localisation across mucosal cell types evidence_span: {"source_cache": "artifacts/acetate-research/16453106.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14165574bceda6c6197de30baae79895b87d2b95272ea42c231554d7a4c015d2", "start_char": 0, "end_char": 1605, "text_sha256": "14165574bceda6c6197de30baae79895b87d2b95272ea42c231554d7a4c015d2"} [acetate-p16453106] Short-chain fatty acid receptor, GPR43, is expressed by enteroendocrine cells and mucosal mast cells in rat intestine. (2006). https://pubmed.ncbi.nlm.nih.gov/16453106/ DOI: 10.1007/s00441-005-0140-x
Complete structured claim and evidence
The FFAR3 reporter was strongly expressed in all cholecystokinin, glucose-dependent insulinotropic peptide and secretin cells of the proximal small intestine, in all GLP-1, peptide YY and neurotensin cells of the distal small intestine, and in the large population of peptide YY and GLP-1 cells throughout the colon and rectum, and also in the neuronal cells of the submucosal and myenteric ganglia.
Human free fatty acid receptor 3 / FFAR3 → Enteroendocrine cell source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/23885020.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b834455e11c2b8fa3c4c19c5d01375815e46c3b0f8e25eb184f0eaa6a51c749e", "start_char": 0, "end_char": 2144, "text_sha256": "b834455e11c2b8fa3c4c19c5d01375815e46c3b0f8e25eb184f0eaa6a51c749e"}
experimental_model
Transgenic monomeric red fluorescent protein reporter mice with FACS purification and quantitative PCR
exposure
Cell-type resolved expression of FFAR2 and FFAR3 reporters, with receptor-specific synthetic agonists on colonic crypt cultures
limitations
Reporter expression is not the same as receptor protein. The FFAR2 result here is weaker in enteroendocrine cells than the rat immunohistochemistry in this collection reports.
nutrient_topic
Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
organism
Mouse
plain_language
The FFAR3 reporter marks nearly every hormone-making cell of the gut, and the gut nerves as well.
primary_references
[acetate-p23885020] GPR41/FFAR3 and GPR43/FFAR2 as cosensors for short-chain fatty acids in enteroendocrine cells vs FFAR3 in enteric neurons and FFAR2 in enteric leukocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/23885020/ DOI: 10.1210/en.2013-1142
tissue_or_cell_type
Whole gastrointestinal tract
Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 290–301
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transgenic monomeric red fluorescent protein reporter mice with FACS purification and quantitative PCR · source_derived_draft · unverified_draft
### acetate-ffar3-on-l-cells The FFAR3 reporter was strongly expressed in all cholecystokinin, glucose-dependent insulinotropic peptide and secretin cells of the proximal small intestine, in all GLP-1, peptide YY and neurotensin cells of the distal small intestine, and in the large population of peptide YY and GLP-1 cells throughout the colon and rectum, and also in the neuronal cells of the submucosal and myenteric ganglia. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: The FFAR3 reporter marks nearly every hormone-making cell of the gut, and the gut nerves as well. organism: Mouse tissue_or_cell_type: Whole gastrointestinal tract experimental_model: Transgenic monomeric red fluorescent protein reporter mice with FACS purification and quantitative PCR limitations: Reporter expression is not the same as receptor protein. The FFAR2 result here is weaker in enteroendocrine cells than the rat immunohistochemistry in this collection reports. exposure: Cell-type resolved expression of FFAR2 and FFAR3 reporters, with receptor-specific synthetic agonists on colonic crypt cultures evidence_span: {"source_cache": "artifacts/acetate-research/23885020.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b834455e11c2b8fa3c4c19c5d01375815e46c3b0f8e25eb184f0eaa6a51c749e", "start_char": 0, "end_char": 2144, "text_sha256": "b834455e11c2b8fa3c4c19c5d01375815e46c3b0f8e25eb184f0eaa6a51c749e"} [acetate-p23885020] GPR41/FFAR3 and GPR43/FFAR2 as cosensors for short-chain fatty acids in enteroendocrine cells vs FFAR3 in enteric neurons and FFAR2 in enteric leukocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/23885020/ DOI: 10.1210/en.2013-1142
Complete structured claim and evidence
The FFAR2 reporter was strongly expressed in a large population of leukocytes in the lamina propria, particularly of the small intestine, but surprisingly only weakly in a subpopulation of enteroendocrine cells; nevertheless synthetic ligands specific for either FFAR3 or FFAR2 each released GLP-1 from colonic crypt cultures.
Human free fatty acid receptor 2 / FFAR2 → Leukocyte of the intestinal lamina propria source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/23885020.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b834455e11c2b8fa3c4c19c5d01375815e46c3b0f8e25eb184f0eaa6a51c749e", "start_char": 0, "end_char": 2144, "text_sha256": "b834455e11c2b8fa3c4c19c5d01375815e46c3b0f8e25eb184f0eaa6a51c749e"}
experimental_model
Transgenic monomeric red fluorescent protein reporter mice with FACS purification and quantitative PCR
exposure
Cell-type resolved expression of FFAR2 and FFAR3 reporters, with receptor-specific synthetic agonists on colonic crypt cultures
limitations
Reporter expression is not the same as receptor protein. The FFAR2 result here is weaker in enteroendocrine cells than the rat immunohistochemistry in this collection reports.
nutrient_topic
Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
organism
Mouse
plain_language
FFAR2 turned out to sit mainly on immune cells rather than on the hormone cells, though its agonist still released the hormone.
primary_references
[acetate-p23885020] GPR41/FFAR3 and GPR43/FFAR2 as cosensors for short-chain fatty acids in enteroendocrine cells vs FFAR3 in enteric neurons and FFAR2 in enteric leukocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/23885020/ DOI: 10.1210/en.2013-1142
tissue_or_cell_type
Whole gastrointestinal tract
Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 303–314
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transgenic monomeric red fluorescent protein reporter mice with FACS purification and quantitative PCR · source_derived_draft · unverified_draft
### acetate-ffar2-mostly-leukocytes The FFAR2 reporter was strongly expressed in a large population of leukocytes in the lamina propria, particularly of the small intestine, but surprisingly only weakly in a subpopulation of enteroendocrine cells; nevertheless synthetic ligands specific for either FFAR3 or FFAR2 each released GLP-1 from colonic crypt cultures. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: FFAR2 turned out to sit mainly on immune cells rather than on the hormone cells, though its agonist still released the hormone. organism: Mouse tissue_or_cell_type: Whole gastrointestinal tract experimental_model: Transgenic monomeric red fluorescent protein reporter mice with FACS purification and quantitative PCR limitations: Reporter expression is not the same as receptor protein. The FFAR2 result here is weaker in enteroendocrine cells than the rat immunohistochemistry in this collection reports. exposure: Cell-type resolved expression of FFAR2 and FFAR3 reporters, with receptor-specific synthetic agonists on colonic crypt cultures evidence_span: {"source_cache": "artifacts/acetate-research/23885020.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b834455e11c2b8fa3c4c19c5d01375815e46c3b0f8e25eb184f0eaa6a51c749e", "start_char": 0, "end_char": 2144, "text_sha256": "b834455e11c2b8fa3c4c19c5d01375815e46c3b0f8e25eb184f0eaa6a51c749e"} [acetate-p23885020] GPR41/FFAR3 and GPR43/FFAR2 as cosensors for short-chain fatty acids in enteroendocrine cells vs FFAR3 in enteric neurons and FFAR2 in enteric leukocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/23885020/ DOI: 10.1210/en.2013-1142
Complete structured claim and evidence
Propionate stimulated secretion of both peptide YY and GLP-1 from wild-type murine colonic crypt cultures and this effect was significantly attenuated in cultures from FFA2 knockout mice, while intra-colonic infusion of propionate elevated both hormones in portal vein plasma in rats and mice but did not significantly stimulate their release in FFA2 knockout mice.
Human free fatty acid receptor 2 / FFAR2 → Plasma GLP-1 response in the specified meal or glucose challenge source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/25109781.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c3c934644f9308be7b2c26f969858debd0d1dbf19bee7e307e529d392fe135d6", "start_char": 0, "end_char": 1621, "text_sha256": "c3c934644f9308be7b2c26f969858debd0d1dbf19bee7e307e529d392fe135d6"}
experimental_model
Wistar rats, C57BL6 mice and FFA2 knockout mice, with colonic crypt cultures and portal vein sampling
exposure
Propionate applied to colonic crypt cultures and infused into the colon, with FFA2 deletion as the test of mediation
limitations
Establishes the receptor-to-hormone step in rodents using propionate rather than acetate. The knockout is the strength of the design.
nutrient_topic
Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
organism
Rat and mouse
plain_language
In rodents the receptor is what releases the two gut hormones; delete it and the response goes.
primary_references
[acetate-p25109781] The short chain fatty acid propionate stimulates GLP-1 and PYY secretion via free fatty acid receptor 2 in rodents. (2015). https://pubmed.ncbi.nlm.nih.gov/25109781/ DOI: 10.1038/ijo.2014.153
tissue_or_cell_type
Colon
Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 316–327
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Wistar rats, C57BL6 mice and FFA2 knockout mice, with colonic crypt cultures and portal vein sampling · source_derived_draft · unverified_draft
### acetate-scfa-glp1-rodent Propionate stimulated secretion of both peptide YY and GLP-1 from wild-type murine colonic crypt cultures and this effect was significantly attenuated in cultures from FFA2 knockout mice, while intra-colonic infusion of propionate elevated both hormones in portal vein plasma in rats and mice but did not significantly stimulate their release in FFA2 knockout mice. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: In rodents the receptor is what releases the two gut hormones; delete it and the response goes. organism: Rat and mouse tissue_or_cell_type: Colon experimental_model: Wistar rats, C57BL6 mice and FFA2 knockout mice, with colonic crypt cultures and portal vein sampling limitations: Establishes the receptor-to-hormone step in rodents using propionate rather than acetate. The knockout is the strength of the design. exposure: Propionate applied to colonic crypt cultures and infused into the colon, with FFA2 deletion as the test of mediation evidence_span: {"source_cache": "artifacts/acetate-research/25109781.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c3c934644f9308be7b2c26f969858debd0d1dbf19bee7e307e529d392fe135d6", "start_char": 0, "end_char": 1621, "text_sha256": "c3c934644f9308be7b2c26f969858debd0d1dbf19bee7e307e529d392fe135d6"} [acetate-p25109781] The short chain fatty acid propionate stimulates GLP-1 and PYY secretion via free fatty acid receptor 2 in rodents. (2015). https://pubmed.ncbi.nlm.nih.gov/25109781/ DOI: 10.1038/ijo.2014.153
Complete structured claim and evidence
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.
Acetate → Plasma GLP-1 response in the specified meal or glucose challenge source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/29494208.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9f8def7b832fdd5d5aed67891c84b18b597d558d9361a92412ccc44264b88126", "start_char": 0, "end_char": 2445, "text_sha256": "9f8def7b832fdd5d5aed67891c84b18b597d558d9361a92412ccc44264b88126"}
experimental_model
Isolated perfused rat colon with luminal and vascular short-chain fatty acid infusion and receptor pharmacology
exposure
Acetate, propionate and butyrate perfused luminally or vascularly, with FFAR2/FFAR3 agonists, an FFAR3 antagonist, nifedipine, diazoxide and 2,4-dinitrophenol
limitations
An isolated organ preparation with an intact blood supply. It reaches the opposite mechanistic conclusion from the knockout work in this collection and is why the receptor route is recorded as disputed.
nutrient_topic
Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
organism
Rat
plain_language
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
Complete structured claim and evidence
A FFAR2- and FFAR3-specific agonist had no effect on colonic GLP-1 output and a FFAR3 antagonist did not decrease the short-chain fatty acid-induced GLP-1 response, whereas the calcium channel blocker nifedipine, the KATP-channel opener diazoxide and the ATP synthesis inhibitor 2,4-dinitrophenol completely abolished the responses, leading the authors to conclude that the fatty acids are metabolised and function as a colonocyte energy source rather than acting through the receptors.
Human free fatty acid receptor 2 / FFAR2 → Plasma GLP-1 response in the specified meal or glucose challenge source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/29494208.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9f8def7b832fdd5d5aed67891c84b18b597d558d9361a92412ccc44264b88126", "start_char": 0, "end_char": 2445, "text_sha256": "9f8def7b832fdd5d5aed67891c84b18b597d558d9361a92412ccc44264b88126"}
experimental_model
Isolated perfused rat colon with luminal and vascular short-chain fatty acid infusion and receptor pharmacology
exposure
Acetate, propionate and butyrate perfused luminally or vascularly, with FFAR2/FFAR3 agonists, an FFAR3 antagonist, nifedipine, diazoxide and 2,4-dinitrophenol
limitations
An isolated organ preparation with an intact blood supply. It reaches the opposite mechanistic conclusion from the knockout work in this collection and is why the receptor route is recorded as disputed.
nutrient_topic
Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
organism
Rat
plain_language
Blocking the receptors changed nothing, while blocking energy production abolished the response.
primary_references
[acetate-p29494208] The impact of short-chain fatty acids on GLP-1 and PYY secretion from the isolated perfused rat colon. (2018). https://pubmed.ncbi.nlm.nih.gov/29494208/ DOI: 10.1152/ajpgi.00346.2017
tissue_or_cell_type
Colon
Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 342–353
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated perfused rat colon with luminal and vascular short-chain fatty acid infusion and receptor pharmacology · source_derived_draft · unverified_draft
### acetate-receptor-not-required A FFAR2- and FFAR3-specific agonist had no effect on colonic GLP-1 output and a FFAR3 antagonist did not decrease the short-chain fatty acid-induced GLP-1 response, whereas the calcium channel blocker nifedipine, the KATP-channel opener diazoxide and the ATP synthesis inhibitor 2,4-dinitrophenol completely abolished the responses, leading the authors to conclude that the fatty acids are metabolised and function as a colonocyte energy source rather than acting through the receptors. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: Blocking the receptors changed nothing, while blocking energy production abolished the response. organism: Rat tissue_or_cell_type: Colon experimental_model: Isolated perfused rat colon with luminal and vascular short-chain fatty acid infusion and receptor pharmacology limitations: An isolated organ preparation with an intact blood supply. It reaches the opposite mechanistic conclusion from the knockout work in this collection and is why the receptor route is recorded as disputed. exposure: Acetate, propionate and butyrate perfused luminally or vascularly, with FFAR2/FFAR3 agonists, an FFAR3 antagonist, nifedipine, diazoxide and 2,4-dinitrophenol evidence_span: {"source_cache": "artifacts/acetate-research/29494208.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9f8def7b832fdd5d5aed67891c84b18b597d558d9361a92412ccc44264b88126", "start_char": 0, "end_char": 2445, "text_sha256": "9f8def7b832fdd5d5aed67891c84b18b597d558d9361a92412ccc44264b88126"} [acetate-p29494208] The impact of short-chain fatty acids on GLP-1 and PYY secretion from the isolated perfused rat colon. (2018). https://pubmed.ncbi.nlm.nih.gov/29494208/ DOI: 10.1152/ajpgi.00346.2017
Complete structured claim and evidence
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.
Acetate → Human free fatty acid receptor 2 / FFAR2 source_derived_draftungraded
Experimental context and source evidence
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
Complete structured claim and evidence
Inulin but not resistant starch significantly increased the short-chain fatty acid area under the curve from 4 to 6 hours, yet neither affected the GLP-1 or PYY area under the curve, while ghrelin at 6 hours after inulin was significantly lower than after glucose and the change in short-chain fatty acid area was negatively related to the change in ghrelin area; responses did not differ significantly between lean and overweight subjects.
Inulin → Plasma GLP-1 response in the specified meal or glucose challenge source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/27966574.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c0282e2d96baff8a6dde713af91c9df8641d7075c78cf1453ee7d74f6016cd3", "start_char": 0, "end_char": 1724, "text_sha256": "7c0282e2d96baff8a6dde713af91c9df8641d7075c78cf1453ee7d74f6016cd3"}
experimental_model
Randomised single-blind crossover in 13 overweight or obese and 12 lean humans
exposure
75 g glucose alone, or with 24 g inulin or 28.2 g resistant starch, with blood sampled over 6 hours
limitations
The ligand did rise: inulin significantly increased the 4 to 6 hour short-chain fatty acid area under the curve. The authors note that a longer adaptation or a larger sample might give a different answer.
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
In people the fatty acids rose and the two appetite hormones did not move, though ghrelin fell.
primary_references
[acetate-p27966574] Acute increases in serum colonic short-chain fatty acids elicited by inulin do not increase GLP-1 or PYY responses but may reduce ghrelin in lean and overweight humans. (2017). https://pubmed.ncbi.nlm.nih.gov/27966574/ DOI: 10.1038/ejcn.2016.249
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 368–379
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised single-blind crossover in 13 overweight or obese and 12 lean humans · source_derived_draft · unverified_draft
### acetate-no-human-glp1 Inulin but not resistant starch significantly increased the short-chain fatty acid area under the curve from 4 to 6 hours, yet neither affected the GLP-1 or PYY area under the curve, while ghrelin at 6 hours after inulin was significantly lower than after glucose and the change in short-chain fatty acid area was negatively related to the change in ghrelin area; responses did not differ significantly between lean and overweight subjects. 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 people the fatty acids rose and the two appetite hormones did not move, though ghrelin fell. organism: Human tissue_or_cell_type: Whole body experimental_model: Randomised single-blind crossover in 13 overweight or obese and 12 lean humans limitations: The ligand did rise: inulin significantly increased the 4 to 6 hour short-chain fatty acid area under the curve. The authors note that a longer adaptation or a larger sample might give a different answer. exposure: 75 g glucose alone, or with 24 g inulin or 28.2 g resistant starch, with blood sampled over 6 hours evidence_span: {"source_cache": "artifacts/acetate-research/27966574.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c0282e2d96baff8a6dde713af91c9df8641d7075c78cf1453ee7d74f6016cd3", "start_char": 0, "end_char": 1724, "text_sha256": "7c0282e2d96baff8a6dde713af91c9df8641d7075c78cf1453ee7d74f6016cd3"} [acetate-p27966574] Acute increases in serum colonic short-chain fatty acids elicited by inulin do not increase GLP-1 or PYY responses but may reduce ghrelin in lean and overweight humans. (2017). https://pubmed.ncbi.nlm.nih.gov/27966574/ DOI: 10.1038/ejcn.2016.249
Complete structured claim and evidence
GPR43 knockout mice had lower levels of intestinal IgA and of IgA-coated gut bacteria than wild-type mice, and feeding wild-type but not GPR43 knockout mice acetate, but not butyrate, promoted the intestinal IgA response independently of T cells.
Acetate → Intestinal immunoglobulin A response to the microbiota source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/27966553.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac", "start_char": 0, "end_char": 1363, "text_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac"}
experimental_model
GPR43 knockout mice with B-cell and dendritic-cell coculture and retinoic acid signalling blockade
exposure
Dietary acetate or butyrate in wild-type and GPR43 knockout mice, with in vitro IgA class switching assays
limitations
A clean set of controls: butyrate did not substitute for acetate, the effect was independent of T cells, and blocking the downstream vitamin A metabolite removed it.
nutrient_topic
Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
organism
Mouse
plain_language
Acetate tells the gut to make the antibody that coats its own bacteria, and butyrate does not stand in for it.
primary_references
[acetate-p27966553] Microbiota metabolite short-chain fatty acid acetate promotes intestinal IgA response to microbiota which is mediated by GPR43. (2017). https://pubmed.ncbi.nlm.nih.gov/27966553/ DOI: 10.1038/mi.2016.114
tissue_or_cell_type
Intestinal mucosa
Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 381–392
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GPR43 knockout mice with B-cell and dendritic-cell coculture and retinoic acid signalling blockade · source_derived_draft · unverified_draft
### acetate-acetate-iga GPR43 knockout mice had lower levels of intestinal IgA and of IgA-coated gut bacteria than wild-type mice, and feeding wild-type but not GPR43 knockout mice acetate, but not butyrate, promoted the intestinal IgA response independently of T cells. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: Acetate tells the gut to make the antibody that coats its own bacteria, and butyrate does not stand in for it. organism: Mouse tissue_or_cell_type: Intestinal mucosa experimental_model: GPR43 knockout mice with B-cell and dendritic-cell coculture and retinoic acid signalling blockade limitations: A clean set of controls: butyrate did not substitute for acetate, the effect was independent of T cells, and blocking the downstream vitamin A metabolite removed it. exposure: Dietary acetate or butyrate in wild-type and GPR43 knockout mice, with in vitro IgA class switching assays evidence_span: {"source_cache": "artifacts/acetate-research/27966553.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac", "start_char": 0, "end_char": 1363, "text_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac"} [acetate-p27966553] Microbiota metabolite short-chain fatty acid acetate promotes intestinal IgA response to microbiota which is mediated by GPR43. (2017). https://pubmed.ncbi.nlm.nih.gov/27966553/ DOI: 10.1038/mi.2016.114
Complete structured claim and evidence
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.
Acetate → Aldehyde dehydrogenase 1A2 / ALDH1A2 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/27966553.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac", "start_char": 0, "end_char": 1363, "text_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac"}
experimental_model
GPR43 knockout mice with B-cell and dendritic-cell coculture and retinoic acid signalling blockade
exposure
Dietary acetate or butyrate in wild-type and GPR43 knockout mice, with in vitro IgA class switching assays
limitations
A clean set of controls: butyrate did not substitute for acetate, the effect was independent of T cells, and blocking the downstream vitamin A metabolite removed it.
nutrient_topic
Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
organism
Mouse
plain_language
Acetate 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
Complete structured claim and evidence
Fasting plasma glucose and HbA1c levels were lower in KK-Ay mice fed 0.3% acetic acid for 8 weeks than in control mice, and acetic acid also reduced the expression of genes involved in gluconeogenesis and lipogenesis, which is in part regulated by AMP-activated protein kinase in the liver.
Acetic acid → Fasting plasma glucose source_derived_draftungraded
Experimental context and source evidence
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"}
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
plain_language
Eight weeks of dietary acid lowered fasting glucose and long-term glucose control, and turned down the liver genes that make glucose and fat.
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 407–418
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-acetic-acid-ampk Fasting plasma glucose and HbA1c levels were lower in KK-Ay mice fed 0.3% acetic acid for 8 weeks than in control mice, and acetic acid also reduced the expression of genes involved in gluconeogenesis and lipogenesis, which is in part regulated by AMP-activated protein kinase 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: Eight weeks of dietary acid lowered fasting glucose and long-term glucose control, and turned down the liver genes that make glucose and fat. organism: Mouse 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
Complete structured claim and evidence
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.
Acetate → AMP-activated protein kinase complexes source_derived_draftungraded
Experimental context and source evidence
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"}
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
Complete structured claim and evidence
The 0.2 g acetic acid group had significantly greater liver and gastrocnemius muscle glycogen concentration than the control group, and the authors concluded that a diet containing acetic acid may enhance glycogen repletion in liver and skeletal muscle.
Acetic acid → Liver glycogen concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/11435516.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e", "start_char": 0, "end_char": 1638, "text_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e"}
experimental_model
Food-deprived rats given graded dietary acetic acid for 2 hours
exposure
0, 0.1, 0.2 or 0.4 g acetic acid per 100 g diet for 2 hours after 15 hours of food deprivation
limitations
Only the 0.2 g dose reached significance for glycogen, so the dose-response is not monotonic. The glycolytic mechanism is the authors’ inference from metabolite ratios, not a direct enzyme 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
Rat
plain_language
A small dose of the acid helped both the liver and the muscle refill their glucose stores.
primary_references
[acetate-p11435516] Acetic acid feeding enhances glycogen repletion in liver and skeletal muscle of rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11435516/ DOI: 10.1093/jn/131.7.1973
tissue_or_cell_type
Liver and 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 433–444
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Food-deprived rats given graded dietary acetic acid for 2 hours · source_derived_draft · unverified_draft
### acetate-acetate-glycogen The 0.2 g acetic acid group had significantly greater liver and gastrocnemius muscle glycogen concentration than the control group, and the authors concluded that a diet containing acetic acid may enhance glycogen repletion in liver and skeletal muscle. 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 small dose of the acid helped both the liver and the muscle refill their glucose stores. organism: Rat tissue_or_cell_type: Liver and skeletal muscle experimental_model: Food-deprived rats given graded dietary acetic acid for 2 hours limitations: Only the 0.2 g dose reached significance for glycogen, so the dose-response is not monotonic. The glycolytic mechanism is the authors’ inference from metabolite ratios, not a direct enzyme measurement. exposure: 0, 0.1, 0.2 or 0.4 g acetic acid per 100 g diet for 2 hours after 15 hours of food deprivation evidence_span: {"source_cache": "artifacts/acetate-research/11435516.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e", "start_char": 0, "end_char": 1638, "text_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e"} [acetate-p11435516] Acetic acid feeding enhances glycogen repletion in liver and skeletal muscle of rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11435516/ DOI: 10.1093/jn/131.7.1973
Complete structured claim and evidence
In liver the concentration of xylulose-5-phosphate was significantly higher in the control group than in the acetic acid groups, and in gastrocnemius muscle the ratio of fructose-1,6-bisphosphate to fructose-6-phosphate was significantly higher in the control group; the authors proposed that acetic acid may activate gluconeogenesis and inactivate glycolysis in liver through suppression of xylulose-5-phosphate accumulation, and inhibit glycolysis in skeletal muscle by suppressing phosphofructokinase-1 activity.
Acetic acid → Glycolysis source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/acetate-research/11435516.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e", "start_char": 0, "end_char": 1638, "text_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e"}
experimental_model
Food-deprived rats given graded dietary acetic acid for 2 hours
exposure
0, 0.1, 0.2 or 0.4 g acetic acid per 100 g diet for 2 hours after 15 hours of food deprivation
limitations
Only the 0.2 g dose reached significance for glycogen, so the dose-response is not monotonic. The glycolytic mechanism is the authors’ inference from metabolite ratios, not a direct enzyme 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
Rat
plain_language
The acid appears to slow the burning of glucose, which is why more of it ends up stored.
primary_references
[acetate-p11435516] Acetic acid feeding enhances glycogen repletion in liver and skeletal muscle of rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11435516/ DOI: 10.1093/jn/131.7.1973
tissue_or_cell_type
Liver and 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 446–457
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Food-deprived rats given graded dietary acetic acid for 2 hours · source_derived_draft · unverified_draft
### acetate-acetate-inhibits-glycolysis In liver the concentration of xylulose-5-phosphate was significantly higher in the control group than in the acetic acid groups, and in gastrocnemius muscle the ratio of fructose-1,6-bisphosphate to fructose-6-phosphate was significantly higher in the control group; the authors proposed that acetic acid may activate gluconeogenesis and inactivate glycolysis in liver through suppression of xylulose-5-phosphate accumulation, and inhibit glycolysis in skeletal muscle by suppressing phosphofructokinase-1 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: The acid appears to slow the burning of glucose, which is why more of it ends up stored. organism: Rat tissue_or_cell_type: Liver and skeletal muscle experimental_model: Food-deprived rats given graded dietary acetic acid for 2 hours limitations: Only the 0.2 g dose reached significance for glycogen, so the dose-response is not monotonic. The glycolytic mechanism is the authors’ inference from metabolite ratios, not a direct enzyme measurement. exposure: 0, 0.1, 0.2 or 0.4 g acetic acid per 100 g diet for 2 hours after 15 hours of food deprivation evidence_span: {"source_cache": "artifacts/acetate-research/11435516.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e", "start_char": 0, "end_char": 1638, "text_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e"} [acetate-p11435516] Acetic acid feeding enhances glycogen repletion in liver and skeletal muscle of rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11435516/ DOI: 10.1093/jn/131.7.1973
Complete structured claim and evidence
At 4 hours after the start of feeding the acetic acid group had significantly greater liver and gastrocnemius muscle glycogen concentrations, and the authors concluded that a diet containing acetic acid may enhance glycogen repletion but not induce supercompensation, the large increase in glycogen that is beneficial in improving performance, by transitory inhibition of glycolysis.
Acetic acid → Gastrocnemius muscle glycogen concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
Rats meal-fed once daily for 10 days, then sampled 4, 8 or 24 hours after feeding
exposure
0.7 g/kg-diet acetic acid in a 9 g meal, with sampling across the daily cycle
limitations
Adds the time dimension that single-timepoint studies miss. The effects were present at 4 hours and the authors explicitly rule out supercompensation.
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 stores refill faster but do not overfill, so this is not carbohydrate loading.
primary_references
[acetate-p16277773] Effect of acetic acid feeding on the circadian changes in glycogen and metabolites of glucose and lipid in liver and skeletal muscle of rats. (2005). https://pubmed.ncbi.nlm.nih.gov/16277773/ DOI: 10.1079/bjn20051545
tissue_or_cell_type
Liver and 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 459–470
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats meal-fed once daily for 10 days, then sampled 4, 8 or 24 hours after feeding · source_derived_draft · unverified_draft
### acetate-no-supercompensation At 4 hours after the start of feeding the acetic acid group had significantly greater liver and gastrocnemius muscle glycogen concentrations, and the authors concluded that a diet containing acetic acid may enhance glycogen repletion but not induce supercompensation, the large increase in glycogen that is beneficial in improving performance, by transitory inhibition of glycolysis. 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 stores refill faster but do not overfill, so this is not carbohydrate loading. organism: Rat tissue_or_cell_type: Liver and skeletal muscle experimental_model: Rats meal-fed once daily for 10 days, then sampled 4, 8 or 24 hours after feeding limitations: Adds the time dimension that single-timepoint studies miss. The effects were present at 4 hours and the authors explicitly rule out supercompensation. exposure: 0.7 g/kg-diet acetic acid in a 9 g meal, with sampling across the daily cycle evidence_span: {"source_cache": "artifacts/acetate-research/16277773.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "305aa81aca9908a350132a7c7dcc42c86be0b6030c70f51b5fe0c8971e75bcfe", "start_char": 0, "end_char": 1594, "text_sha256": "305aa81aca9908a350132a7c7dcc42c86be0b6030c70f51b5fe0c8971e75bcfe"} [acetate-p16277773] Effect of acetic acid feeding on the circadian changes in glycogen and metabolites of glucose and lipid in liver and skeletal muscle of rats. (2005). https://pubmed.ncbi.nlm.nih.gov/16277773/ DOI: 10.1079/bjn20051545
Complete structured claim and evidence
At 4 hours after feeding, liver malonyl-CoA, an allosteric inhibitor of carnitine palmitoyl-transferase, was significantly lower in the acetic acid group than in the control group, along with a lower serum lactate concentration and a lower ratio of insulin to glucagon, indicating the possibility of a transient enhancement of fatty acid oxidation in liver.
Acetic acid → Malonyl-CoA source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
Rats meal-fed once daily for 10 days, then sampled 4, 8 or 24 hours after feeding
exposure
0.7 g/kg-diet acetic acid in a 9 g meal, with sampling across the daily cycle
limitations
Adds the time dimension that single-timepoint studies miss. The effects were present at 4 hours and the authors explicitly rule out supercompensation.
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 brake on fat burning came off for a few hours.
primary_references
[acetate-p16277773] Effect of acetic acid feeding on the circadian changes in glycogen and metabolites of glucose and lipid in liver and skeletal muscle of rats. (2005). https://pubmed.ncbi.nlm.nih.gov/16277773/ DOI: 10.1079/bjn20051545
tissue_or_cell_type
Liver and 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 472–483
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats meal-fed once daily for 10 days, then sampled 4, 8 or 24 hours after feeding · source_derived_draft · unverified_draft
### acetate-malonyl-coa-fall At 4 hours after feeding, liver malonyl-CoA, an allosteric inhibitor of carnitine palmitoyl-transferase, was significantly lower in the acetic acid group than in the control group, along with a lower serum lactate concentration and a lower ratio of insulin to glucagon, indicating the possibility of a transient enhancement of fatty acid oxidation in 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 brake on fat burning came off for a few hours. organism: Rat tissue_or_cell_type: Liver and skeletal muscle experimental_model: Rats meal-fed once daily for 10 days, then sampled 4, 8 or 24 hours after feeding limitations: Adds the time dimension that single-timepoint studies miss. The effects were present at 4 hours and the authors explicitly rule out supercompensation. exposure: 0.7 g/kg-diet acetic acid in a 9 g meal, with sampling across the daily cycle evidence_span: {"source_cache": "artifacts/acetate-research/16277773.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "305aa81aca9908a350132a7c7dcc42c86be0b6030c70f51b5fe0c8971e75bcfe", "start_char": 0, "end_char": 1594, "text_sha256": "305aa81aca9908a350132a7c7dcc42c86be0b6030c70f51b5fe0c8971e75bcfe"} [acetate-p16277773] Effect of acetic acid feeding on the circadian changes in glycogen and metabolites of glucose and lipid in liver and skeletal muscle of rats. (2005). https://pubmed.ncbi.nlm.nih.gov/16277773/ DOI: 10.1079/bjn20051545
Complete structured claim and evidence
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.
Intravenous sodium acetate infusion → Active-form pyruvate dehydrogenase in skeletal muscle source_derived_draftungraded
Experimental context and source evidence
evidence_span
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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
Complete structured claim and evidence
During exercise acetyl-CoA, citrate and the acetyl-CoA to free CoA ratio were further elevated and the differences present at rest were resolved, with active-form pyruvate dehydrogenase increasing to the same extent with acetate and with the control infusion, so that during exercise its regulation appeared independent of variations in the acetyl-CoA to free CoA ratio and acetate infusion was not effective in perturbing the glucose-fatty acid cycle.
Cycling exercise at 40 and 80 percent of maximal oxygen uptake → Active-form pyruvate dehydrogenase in skeletal muscle source_derived_draftungraded
Experimental context and source evidence
evidence_span
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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
During exercise the muscle ignored the extra acetate entirely.
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 498–509
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-exercise-overrides During exercise acetyl-CoA, citrate and the acetyl-CoA to free CoA ratio were further elevated and the differences present at rest were resolved, with active-form pyruvate dehydrogenase increasing to the same extent with acetate and with the control infusion, so that during exercise its regulation appeared independent of variations in the acetyl-CoA to free CoA ratio and acetate infusion was not effective in perturbing the glucose-fatty acid cycle. 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: During exercise the muscle ignored the extra acetate entirely. 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
Complete structured claim and evidence
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.
Recovery of infused carbon label as expired carbon dioxide → De novo lipogenesis source_derived_draftungraded
Experimental context and source evidence
evidence_span
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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
Complete structured claim and evidence
Acetate made a significantly larger carbon contribution to lipids than propionate, butyrate, glucose or glutamine in rat colonic epithelial cells, with butyrate and 3-hydroxybutyrate the other major contributors and glucose, glutamine and propionate making only minor contributions, and incorporation was significantly greater into phospholipids than into free fatty acids and triacylglycerides, suggesting the major role of this lipogenesis is membrane synthesis.
Acetate → De novo lipogenesis source_derived_draftungraded
Experimental context and source evidence
evidence_span
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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
Complete structured claim and evidence
Hydroxycitrate did not affect the incorporation of acetate or butyrate carbon into lipids even though it inhibited colonic ATP-citrate lyase, suggesting that the short-chain fatty acid carbon used in lipid synthesis by colonocytes is not transported to the cytosol as citrate, and that colonocytes synthesise lipids by a pathway distinct from the liver.
Human ATP-citrate lyase / ACLY → De novo lipogenesis source_derived_draftungraded
Experimental context and source evidence
evidence_span
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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
Blocking the usual enzyme changed nothing, so the carbon was arriving another way.
primary_references
[acetate-p14608066] Acetate and butyrate are the major substrates for de novo lipogenesis in rat colonic epithelial cells. (2003). https://pubmed.ncbi.nlm.nih.gov/14608066/ DOI: 10.1093/jn/133.11.3509
tissue_or_cell_type
Colonic epithelium
Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 537–548
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat colonic epithelial cells with competing labelled substrates and ATP-citrate lyase inhibition · source_derived_draft · unverified_draft
### acetate-citrate-route-not-used Hydroxycitrate did not affect the incorporation of acetate or butyrate carbon into lipids even though it inhibited colonic ATP-citrate lyase, suggesting that the short-chain fatty acid carbon used in lipid synthesis by colonocytes is not transported to the cytosol as citrate, and that colonocytes synthesise lipids by a pathway distinct from the liver. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: Blocking the usual enzyme changed nothing, so the carbon was arriving another way. organism: Rat tissue_or_cell_type: Colonic epithelium experimental_model: Rat colonic epithelial cells with competing labelled substrates and ATP-citrate lyase inhibition limitations: An isolated cell measurement. Its ATP-citrate lyase result anticipates by seventeen years the in vivo finding in this collection that lipogenic acetyl-CoA can arrive without that enzyme. exposure: Labelled acetate, propionate, butyrate, 3-hydroxybutyrate, glucose and glutamine, with hydroxycitrate as an ATP-citrate lyase inhibitor evidence_span: {"source_cache": "artifacts/acetate-research/14608066.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b2c891f60d02b85a8f4e87f26751f1129b0445fe52fb35ca5e5e20a92d4ecc5a", "start_char": 0, "end_char": 1642, "text_sha256": "b2c891f60d02b85a8f4e87f26751f1129b0445fe52fb35ca5e5e20a92d4ecc5a"} [acetate-p14608066] Acetate and butyrate are the major substrates for de novo lipogenesis in rat colonic epithelial cells. (2003). https://pubmed.ncbi.nlm.nih.gov/14608066/ DOI: 10.1093/jn/133.11.3509
Complete structured claim and evidence
Using in vivo isotope tracing, liver-specific deletion of Acly in mice was unable to suppress fructose-induced lipogenesis.
Liver-specific ATP citrate lyase knockout mouse genotype → De novo lipogenesis source_derived_draftungraded
Experimental context and source evidence
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
Deleting the enzyme everyone assumed was responsible did not stop the fat being made.
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 550–561
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-acly-deletion-insufficient Using in vivo isotope tracing, liver-specific deletion of Acly in mice was unable to suppress fructose-induced lipogenesis. 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: Deleting the enzyme everyone assumed was responsible did not stop the fat being made. 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
Complete structured claim and evidence
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.
Acetate produced from dietary fructose by the gut microbiota → De novo lipogenesis source_derived_draftungraded
Experimental context and source evidence
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
Complete structured claim and evidence
When fructose is consumed more gradually to facilitate its absorption in the small intestine, both citrate cleavage in hepatocytes and microorganism-derived acetate contribute to lipogenesis, whereas the lipogenic transcriptional program is activated in response to fructose independently of acetyl-CoA metabolism, revealing a two-pronged mechanism in which fructolysis within hepatocytes provides the signal to express lipogenic genes while microbial acetate feeds the lipogenic acetyl-CoA pools.
Fructose consumed as a single bolus rather than gradually → De novo lipogenesis source_derived_draftungraded
Experimental context and source evidence
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
How fast the sugar is eaten decides which of the two routes supplies the carbon; the signal that switches the genes on is separate from either.
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
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 576–587
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-intake-rate-decides When fructose is consumed more gradually to facilitate its absorption in the small intestine, both citrate cleavage in hepatocytes and microorganism-derived acetate contribute to lipogenesis, whereas the lipogenic transcriptional program is activated in response to fructose independently of acetyl-CoA metabolism, revealing a two-pronged mechanism in which fructolysis within hepatocytes provides the signal to express lipogenic genes while microbial acetate feeds the lipogenic acetyl-CoA pools. 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: How fast the sugar is eaten decides which of the two routes supplies the carbon; the signal that switches the genes on is separate from either. 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
Complete structured claim and evidence
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.
Uptake of acetate from outside the cell → Core histone lysine acetylation source_derived_draftungraded
Experimental context and source evidence
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
Complete structured claim and evidence
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.
Chromatin-bound nuclear acetyl-CoA synthetase 2 → Core histone lysine acetylation source_derived_draftungraded
Experimental context and source evidence
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
Complete structured claim and evidence
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.
Acetate derived from hepatic alcohol metabolism → Histone acetylation in brain neurons source_derived_draftungraded
Experimental context and source evidence
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"}
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
Complete structured claim and evidence
In a pregnant mouse, exposure to labelled alcohol resulted in the incorporation of labelled acetyl groups into gestating fetal brains.
Ethanol → Acetyl groups incorporated into gestating fetal brains source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
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"}
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
The same atoms cross into the fetus and land on the chromatin of its developing 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
trigger_kind
biomarker_context 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 628–639
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-maternal-alcohol-fetal-brain In a pregnant mouse, exposure to labelled alcohol resulted in the incorporation of labelled acetyl groups into gestating fetal brains. Condition category: biomarker_context 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 same atoms cross into the fetus and land on the chromatin of its developing 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
Complete structured claim and evidence
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.
Acetate → Transcriptional programs related to learning and memory in hippocampal neurons source_derived_draftungraded
Experimental context and source evidence
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"}
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
Complete structured claim and evidence
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.
Glyceryl triacetate, an oral acetate precursor → Histone acetylation in brain neurons source_derived_draftungraded
Experimental context and source evidence
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
Complete structured claim and evidence
Acetate supplementation had no effect on histone acetyltransferase activity in brain extracts but significantly inhibited histone deacetylase activity twofold at 2 and 4 hours after treatment and decreased HDAC 2 levels at 4 hours, leading the authors to conclude that acetyl-CoA derived from acetate supplementation increases brain histone acetylation state by reducing deacetylase activity and expression.
Glyceryl triacetate, an oral acetate precursor → histone deacetylase activity source_derived_draftungraded
Experimental context and source evidence
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
The marks accumulated because they were being removed more slowly, not because more were being added.
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 667–678
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-inhibits-hdac Acetate supplementation had no effect on histone acetyltransferase activity in brain extracts but significantly inhibited histone deacetylase activity twofold at 2 and 4 hours after treatment and decreased HDAC 2 levels at 4 hours, leading the authors to conclude that acetyl-CoA derived from acetate supplementation increases brain histone acetylation state by reducing deacetylase activity and expression. 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 marks accumulated because they were being removed more slowly, not because more were being added. 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
Complete structured claim and evidence
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.
Acetate → The Drosophila immunodeficiency / IMD signalling pathway source_derived_draftungraded
Experimental context and source evidence
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"}
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
Complete structured claim and evidence
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.
Tarag, a putative Drosophila monocarboxylic acid transporter → Acetate source_derived_draftungraded
Experimental context and source evidence
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"}
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
Complete structured claim and evidence
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.
Acetate → Hypothalamus source_derived_draftungraded
Experimental context and source evidence
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"}
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
Complete structured claim and evidence
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.
Acetate → Appetite source_derived_draftungraded
Experimental context and source evidence
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"}
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
Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

Reading a vinegar effect when the stomach already empties slowly

Condition: biomarker_context · Existing diabetic gastroparesis in type 1 diabetes.

Normal role: Vinegar taken with a meal is reported to slow gastric emptying, which is read as flattening the glucose rise in healthy people.

Recorded consequence: The same slowing is unwanted: the median emptying rate fell from 27% to 17% over two weeks of daily vinegar, which the authors judged a disadvantage for glycaemic control.

Scope: Ten patients with type 1 diabetes, one after vagotomy

When the receptor that senses acetate is absent

Condition: machinery_impairment · GPR43 deficiency in mice, or removal of the microbiota that supplies the ligand.

Normal role: GPR43 on adipocytes senses microbial short-chain fatty acids and suppresses insulin signalling locally, limiting how much fat the tissue takes on.

Recorded consequence: Mice become obese on a normal diet, and the phenotype disappears when there are no gut bacteria to make the signal, which places the cause in the microbial metabolite rather than in the receptor alone.

Scope: Mouse genetics with germ-free and antibiotic controls

When the expected route to lipogenic acetyl-CoA is deleted

Condition: machinery_impairment · Liver-specific deletion of Acly, with microbiota depletion and hepatic ACSS2 silencing as tests of the alternative route.

Normal role: ATP citrate lyase cleaves cytosolic citrate to generate the acetyl-CoA used for making fat, and is upregulated after carbohydrate is eaten.

Recorded consequence: Fructose-induced lipogenesis is not suppressed by deleting ACLY, but is potently suppressed by depleting the microbiota or silencing ACSS2, showing the carbon arrives as microbial acetate instead. When the fructose is eaten gradually rather than as a bolus, both routes contribute.

Scope: Mouse in vivo isotope tracing

The sources

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Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source

Recorded disagreements

Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.

Do short-chain fatty acids raise GLP-1 and PYY, and if so is the receptor involved?Three designs disagree on two separate points. Knockout work in rats and mice found that propionate stimulates GLP-1 and PYY and that deleting FFA2 abolishes the response, placing the effect on the receptor. The isolated perfused rat colon found the opposite pattern: acetate and butyrate released GLP-1 but propionate did not, a receptor-specific synthetic agonist had no effect at all, a receptor antagonist did not block the response, and inhibitors of ATP synthesis abolished it, so those authors concluded the fatty acids act as colonocyte fuel rather than as ligands. A randomised crossover in 25 lean and overweight humans raised serum short-chain fatty acids with inulin and found no change in either hormone, though ghrelin fell. The designs differ in species, in which fatty acid was given, in route, and in whether the tissue was intact and perfused. Receptor pharmacology in the perfused study also found the natural fatty acids to be low-potency partial agonists, around 750-fold weaker than a synthetic full agonist, which bears on whether physiological concentrations could act through the receptor at all. Neither the species question nor the mechanism question is resolved here.Read the recorded disagreement
Does FFAR2 sit on the hormone-secreting cells of the gut, or mainly on immune cells?Immunohistochemistry in rat ileum and colon localised GPR43 to peptide YY-expressing enteroendocrine cells and to mucosal mast cells. A reporter mouse line found the FFAR2 reporter strongly expressed in lamina propria leukocytes and only weakly in a subpopulation of enteroendocrine cells, while the FFAR3 reporter marked nearly all of them. The two disagree on where the receptor mainly is, which matters because the enteroendocrine location is what the gut hormone story rests on. They differ in species and in method, an antiserum against a synthesised fragment against a transgenic fluorescent reporter, and neither measures receptor protein in the other species. Recorded as a difference in what was measured, not resolved.Read the recorded disagreement
Does acetate taken in from outside the cell reach histones in a quantity that matters?Quantitative accounting in cultured cells found that mitochondrial and lipogenic demand for two-carbon acetyl units considerably exceeds the uptake of exogenous acetate, leaving it to contribute only sparingly to histone acetylation; in that system the enzyme maintains histone acetylation mainly by recapturing acetate already released from histones. Against that, in vivo isotope labelling in mice placed acetyl groups derived from alcohol and from injected labelled acetate directly onto brain histones, and a single large oral dose of an acetate precursor in rats raised three specific brain histone marks. The conditions differ sharply: cultured cells at a fixed acetate concentration against whole animals given alcohol or a 6 g/kg precursor dose, which produce far higher blood acetate than a meal does. The rat study also found the marks rose because deacetylation slowed rather than because acetylation increased, which is a different mechanism again. Whether ordinary dietary acetate reaches histones in any meaningful quantity is not settled by these records.Read the recorded disagreement
Does vinegar lower postprandial glucose by delaying gastric emptying?One study inferred delayed gastric emptying from lower paracetamol appearance after a vinegar meal in ten volunteers and concluded that this probably explains the improved glycaemia. A separate design compared native vinegar against the same vinegar neutralised to pH 6.0 and measured gastric emptying directly by ultrasonography: emptying times did not differ between the two, yet only the acid form depressed the glucose response, by 31.4%. Those authors concluded the mechanism is related to acidity but not to gastric emptying. The second design also found that the form which worked better on glucose produced less blood acetate, not more, which argues against the acetate anion being the agent. Against that, it enrolled five subjects for the glucose arm and four for the ultrasound arm, and the two studies used different markers of emptying. Which reading is correct is not established here.Read the recorded disagreement

Open questions in this collection

Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.

Whether the glucose-lowering effect of ingested vinegar is an effect of the acid, of the acetate anion, or of delayed gastric emptying.The neutralised-vinegar study found the acid form lowered glucose while producing less blood acetate and no difference in emptying; the paracetamol study concluded emptying was probably responsible; and the mouse work found the neutralised salt activates AMPK directly in hepatocytes. No record here tests all three against each other.
Whether short-chain fatty acids act on the gut hormone cells through FFAR2 and FFAR3 at all, or simply as colonocyte fuel.Knockout work says the receptor is required; the isolated perfused colon says a receptor-specific agonist does nothing and metabolic inhibitors abolish the response. The same study found the natural fatty acids to be roughly 750-fold weaker than a synthetic full agonist at FFAR2.
How much of human hepatic lipogenesis uses the microbial acetate route rather than ATP citrate lyase.The route was established with bolus fructose in mice using genetic deletion and microbiota depletion, and the same study showed the balance shifts back toward citrate cleavage when fructose is eaten gradually. No record here quantifies either route in people.
Whether acetate reaching the human brain from colonic fermentation is enough to change appetite or histone acetylation at ordinary dietary intakes.The brain uptake, appetite and histone records are rodent and use intraperitoneal acetate, labelled alcohol or a 6 g/kg precursor dose; the human fibre study in this collection raised serum short-chain fatty acids without changing GLP-1 or PYY, and cultured-cell accounting found exogenous acetate contributes only sparingly to histone acetylation.
Whether the acetate-driven immunoglobulin A response depends on vitamin A status.The mechanism runs through dendritic-cell Aldh1a2, which converts vitamin A into retinoic acid, and blocking retinoic acid signalling abolished the effect; no record here tests the pathway against varied vitamin A intake.

Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.

Evidence, AI assistance and curation standards

Acetic acid

The mechanisms

No difference was observed between gastric emptying times after the acetic acid plus bread meal and the sodium acetate plus bread meal, measured by ultrasonography in four subjects.

The presence of acetic acid given as vinegar significantly reduced the postprandial glucose and insulin responses to a starchy meal, with a glycaemic index of 64 and an insulinaemic index of 65 against the white bread reference meal.

As judged from lowered paracetamol levels after the test meal with vinegar, the authors concluded that the mechanism is probably a delayed gastric emptying rate.

The rating of satiety was directly related to the acetic acid level, with a linear dose-response relation, and the highest level of vinegar increased the satiety score at 30, 90 and 120 minutes after the meal.

The glycaemic and insulinaemic indices of cold potatoes with added vinegar were significantly reduced by 43% and 31% respectively compared with freshly boiled potatoes; vinegar was tested only together with cold storage in this design.

Cold storage of boiled potatoes increased resistant starch content significantly from 3.3% to 5.2% on a starch basis, and cold storage on its own lowered the insulinaemic index by 28% compared with freshly boiled potatoes.

In patients with type 1 diabetes and diabetic gastroparesis the median gastric emptying rate was 27% without vinegar and 17% with vinegar, a statistically significant reduction, and the authors concluded this might be a disadvantage for their glycaemic control.

Body weight, body mass index, visceral fat area, waist circumference and serum triglyceride levels were significantly lower in both vinegar intake groups than in the placebo group after 12 weeks.

A 39-year-old woman who drank one tablespoon of white vinegar to soften a crab shell stuck in her throat was found on endoscopy to have inflammation of the oropharynx and second-degree caustic injury of the oesophagus extending to the cardia, with an uneventful recovery.

GPR43-deficient mice were obese on a normal diet whereas mice overexpressing GPR43 specifically in adipose tissue remained lean even when fed a high-fat diet, and raised under germ-free conditions or after treatment with antibiotics both types of mice had a normal phenotype.

Short-chain fatty acid-mediated activation of GPR43 suppressed insulin signalling in adipocytes, which inhibited fat accumulation in adipose tissue and promoted the metabolism of unincorporated lipids and glucose in other tissues, establishing GPR43 as a sensor for excessive dietary energy.

GPR43 immunoreactivity was localised to enteroendocrine cells expressing peptide YY, whereas 5-hydroxytryptamine-immunoreactive enteroendocrine cells were not immunoreactive for GPR43, and mast cells of the lamina propria expressing 5-hydroxytryptamine were also GPR43-immunoreactive.

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.

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.

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.

Fasting plasma glucose and HbA1c levels were lower in KK-Ay mice fed 0.3% acetic acid for 8 weeks than in control mice, and acetic acid also reduced the expression of genes involved in gluconeogenesis and lipogenesis, which is in part regulated by AMP-activated protein kinase in the liver.

The 0.2 g acetic acid group had significantly greater liver and gastrocnemius muscle glycogen concentration than the control group, and the authors concluded that a diet containing acetic acid may enhance glycogen repletion in liver and skeletal muscle.

Using in vivo isotope tracing, liver-specific deletion of Acly in mice was unable to suppress fructose-induced lipogenesis.

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.

In a pregnant mouse, exposure to labelled alcohol resulted in the incorporation of labelled acetyl groups into gestating fetal brains.

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.

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.

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The sources

Recorded disagreements

Open questions in this collection