Component
Human HepG2 ACC phosphorylation
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.
What acts on it
SA increased Human HepG2 ACC phosphorylation.
Experimental context and source evidence
- evidence_access
- Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
- experimental_contrast
- {"intervention": "SA treatment", "comparator": "Matched untreated cells", "endpoint": "SA increased Human HepG2 ACC phosphorylation.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
- experimental_model
- Human HepG2 cell signaling assay.
- interpretation_status
- Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
- limitations
- Context-specific signaling; no asserted mediation of a separate in-vivo lipid effect.
- plain_language
- SA increased Human HepG2 ACC phosphorylation.
- primary_references
- Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC. | 2019 | DOI 10.3390/ijms20030582 | PMID 30700011 | https://pubmed.ncbi.nlm.nih.gov/30700011/ | https://doi.org/10.3390/ijms20030582 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6387373/
- source_locator
- Reviewed reference lines 77-77; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 77–77
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human HepG2 cell signaling assay. · source_derived_draft · unverified_draft
**Lipid accumulation studies identify responses, not direct inhibition.** In HepG2/Huh7 and 3T3-L1 experiments, shikimic acid was associated with lower lipid staining and altered lipogenic proteins, including lower MID1IP1, LXRα and SREBP-1c; AMPKα and ACC phosphorylation increased in the reported cell contexts. Genetic manipulation of MID1IP1 and compound-C experiments probed pathway involvement. These cultured-cell observations do not prove direct binding to MID1IP1, human fatty-liver efficacy, or that AMPK causes the triglyceride change in the separate mouse-feeding study. Individual cell-dose details remain in the original paper rather than being guessed. [Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC.](https://pubmed.ncbi.nlm.nih.gov/30700011/)
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.