Component
Glucose-6-phosphatase
Glucose-6-phosphatase. 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)
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.
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 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.