Component
Acetate derived from hepatic alcohol metabolism
Acetate derived from hepatic alcohol metabolism. Species, exposure and limitations are retained in each linked claim.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
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.
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
Where it participates (unsigned role)
In a pregnant mouse, exposure to labelled alcohol resulted in the incorporation of labelled acetyl groups into gestating fetal brains.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.