Component
GLUT4 recruitment to human adipocyte plasma membrane
GLUT4 recruitment to human adipocyte plasma membrane. Interpret through the linked experimental species, preparation, compartment and exposure; no universal causal effect is implied.
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 acts on it
In human omental adipocytes, 50 uM cyanidin-3-glucoside increased GLUT4 membrane recruitment in the tested culture model.
Experimental context and source evidence
- evidence_access
- Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
- experimental_contrast
- {"intervention": "50 uM cyanidin-3-glucoside", "comparator": "Untreated/vehicle-matched adipocytes in the corresponding assay", "endpoint": "In human omental adipocytes, 50 uM cyanidin-3-glucoside increased GLUT4 membrane recruitment in the tested culture model.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
- experimental_model
- Human omental adipocytes, 18-hour exposure; parallel mouse experiments are separate.
- interpretation_status
- Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
- limitations
- High systemic-exposure model; roughly hundreds-fold above selected free-serum peaks. Does not establish dietary insulin replacement.
- plain_language
- In human omental adipocytes, 50 uM cyanidin-3-glucoside increased GLUT4 membrane recruitment in the tested culture model.
- primary_references
- Cyanidin-3-O-β-glucoside and protocatechuic acid exert insulin-like effects by upregulating PPARγ activity in human omental adipocytes. | 2011 | DOI 10.2337/db10-1461 | PMID 21788573 | https://pubmed.ncbi.nlm.nih.gov/21788573/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/ | https://doi.org/10.2337/db10-1461
- source_locator
- Reviewed reference lines 70-70; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 70–70
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 omental adipocytes, 18-hour exposure; parallel mouse experiments are separate. · source_derived_draft · unverified_draft
**Adipocyte glucose uptake involves PPARγ in one high-exposure model.** Human omental adipocytes exposed to 50 µM C3G or 100 µM PCA showed increased glucose uptake, GLUT4 recruitment and adiponectin-related responses. The decisive PPARγ silencing and antagonist experiments were performed in mouse 3T3-L1 adipocytes: disrupting PPARγ prevented polyphenol-associated GLUT4/adiponectin upregulation and GLUT4 recruitment. These mouse perturbations must not be relabeled human knockdowns. The human-cell concentrations are far above the selected free serum peaks in the tracer study; the experiment does not establish an insulin-like dietary effect. [Scazzocchio et al., 2011](https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/).
Complete structured claim and evidenceIn human omental adipocytes, 100 uM protocatechuic-acid increased GLUT4 membrane recruitment in the tested culture model.
Experimental context and source evidence
- evidence_access
- Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
- experimental_contrast
- {"intervention": "100 uM protocatechuic-acid", "comparator": "Untreated/vehicle-matched adipocytes in the corresponding assay", "endpoint": "In human omental adipocytes, 100 uM protocatechuic-acid increased GLUT4 membrane recruitment in the tested culture model.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
- experimental_model
- Human omental adipocytes, 18-hour exposure; parallel mouse experiments are separate.
- interpretation_status
- Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
- limitations
- High systemic-exposure model; roughly hundreds-fold above selected free-serum peaks. Does not establish dietary insulin replacement.
- plain_language
- In human omental adipocytes, 100 uM protocatechuic-acid increased GLUT4 membrane recruitment in the tested culture model.
- primary_references
- Cyanidin-3-O-β-glucoside and protocatechuic acid exert insulin-like effects by upregulating PPARγ activity in human omental adipocytes. | 2011 | DOI 10.2337/db10-1461 | PMID 21788573 | https://pubmed.ncbi.nlm.nih.gov/21788573/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/ | https://doi.org/10.2337/db10-1461
- source_locator
- Reviewed reference lines 70-70; exact primary location described in quoted passage where extracted.
Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 70–70
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 omental adipocytes, 18-hour exposure; parallel mouse experiments are separate. · source_derived_draft · unverified_draft
**Adipocyte glucose uptake involves PPARγ in one high-exposure model.** Human omental adipocytes exposed to 50 µM C3G or 100 µM PCA showed increased glucose uptake, GLUT4 recruitment and adiponectin-related responses. The decisive PPARγ silencing and antagonist experiments were performed in mouse 3T3-L1 adipocytes: disrupting PPARγ prevented polyphenol-associated GLUT4/adiponectin upregulation and GLUT4 recruitment. These mouse perturbations must not be relabeled human knockdowns. The human-cell concentrations are far above the selected free serum peaks in the tracer study; the experiment does not establish an insulin-like dietary effect. [Scazzocchio et al., 2011](https://pmc.ncbi.nlm.nih.gov/articles/PMC3161313/).
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.