Component
The hepatic lipogenic transcriptional program
The hepatic lipogenic transcriptional program. Species, exposure and limitations are retained in each linked claim.
1 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.
Where it participates (unsigned role)
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.
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
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.