Component
GLUT4 translocation in C2C12 myotubes
Glucose transporter movement to the surface with glucose uptake.
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 C2C12 myotubes lariciresinol activated insulin signalling leading to GLUT4 translocation and augmented glucose uptake.
Experimental context and source evidence
- duration
- Not stated here
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- C2C12 myotubes
- exposure
- Lariciresinol
- limitations
- The enantiomer and the concentrations are not stated in the abstract. The abstract describes insulin signalling and GSK-3β and does not report AMPK.
- organism
- C2C12 myotubes
- plain_language
- In C2C12 myotubes lariciresinol activated insulin signalling leading to GLUT4 translocation and augmented glucose uptake.
- primary_references
- Lariciresinol Displays Anti-Diabetic Activity through Inhibition of α-Glucosidase and Activation and Enhancement of Insulin Signaling. (2022). https://pubmed.ncbi.nlm.nih.gov/35490401/ DOI: 10.1002/mnfr.202100910
- route
- In vitro
- tissue
- Insulin signalling and glucose transporter translocation
Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 176–185
Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft
## lariciresinol-moves-glut4-and-raises-glucose-uptake In C2C12 myotubes lariciresinol activated insulin signalling leading to GLUT4 translocation and augmented glucose uptake. Model/species: C2C12 myotubes Tissue/system: Insulin signalling and glucose transporter translocation Exposure: Lariciresinol Route: In vitro Duration: Not stated here Limits: The enantiomer and the concentrations are not stated in the abstract. The abstract describes insulin signalling and GSK-3β and does not report AMPK. Primary reference: Lariciresinol Displays Anti-Diabetic Activity through Inhibition of α-Glucosidase and Activation and Enhancement of Insulin Signaling. (2022). https://pubmed.ncbi.nlm.nih.gov/35490401/ DOI: 10.1002/mnfr.202100910 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
Complete structured claim and evidence
Where it participates (unsigned role)
Three weeks of oral lariciresinol at 10 mg/kg decreased blood glucose and increased insulin on an oral glucose tolerance test in streptozotocin-treated diabetic mice.
Experimental context and source evidence
- duration
- 3 weeks
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- Streptozotocin-treated diabetic mice
- exposure
- Lariciresinol 10 mg/kg orally for 3 weeks
- limitations
- Streptozotocin-induced diabetes models beta-cell destruction rather than the common human disease, and the enantiomer administered is not stated.
- organism
- Streptozotocin-treated diabetic mice
- plain_language
- Three weeks of oral lariciresinol at 10 mg/kg decreased blood glucose and increased insulin on an oral glucose tolerance test in streptozotocin-treated diabetic mice.
- primary_references
- Lariciresinol Displays Anti-Diabetic Activity through Inhibition of α-Glucosidase and Activation and Enhancement of Insulin Signaling. (2022). https://pubmed.ncbi.nlm.nih.gov/35490401/ DOI: 10.1002/mnfr.202100910
- route
- Oral
- tissue
- Blood glucose, insulin and pancreatic histology
Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 187–196
Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft
## lariciresinol-lowers-blood-glucose-in-diabetic-mice Three weeks of oral lariciresinol at 10 mg/kg decreased blood glucose and increased insulin on an oral glucose tolerance test in streptozotocin-treated diabetic mice. Model/species: Streptozotocin-treated diabetic mice Tissue/system: Blood glucose, insulin and pancreatic histology Exposure: Lariciresinol 10 mg/kg orally for 3 weeks Route: Oral Duration: 3 weeks Limits: Streptozotocin-induced diabetes models beta-cell destruction rather than the common human disease, and the enantiomer administered is not stated. Primary reference: Lariciresinol Displays Anti-Diabetic Activity through Inhibition of α-Glucosidase and Activation and Enhancement of Insulin Signaling. (2022). https://pubmed.ncbi.nlm.nih.gov/35490401/ DOI: 10.1002/mnfr.202100910 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
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.