Component
3-O-Methyl-D-glucose
Transported nonmetabolizable sugar probe, distinct from D-glucose.
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 it acts on
Human erythrocyte and inside-out-vesicle kinetic assays showed DHA and 3-O-methylglucose competing at both membrane faces, consistent with transport through the same GLUT1 complex.
Experimental context and source evidence
- cross_nutrient
- true
- experimental_model
- Human erythrocytes, ghosts and inside-out membrane vesicles
- exposure
- Initial-rate substrate competition and trans-acceleration assays
- limitations
- 3-O-methylglucose is a transport probe, not dietary glucose. This challenges segregated transport pools without denying vitamin C recycling.
- nutrient_topic
- Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
- organism
- Homo sapiens
- plain_language
- A later kinetic study found that sugar and oxidized vitamin C share the red-cell GLUT1 transport pathway.
- primary_references
- [sage2014] Human erythrocytes transport dehydroascorbic acid and sugars using the same transporter complex. (2014). https://pubmed.ncbi.nlm.nih.gov/24598365/ DOI: 10.1152/ajpcell.00044.2014
- tissue_or_cell_type
- Erythrocyte plasma membrane and inside-out vesicles
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 533–544
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human erythrocytes, ghosts and inside-out membrane vesicles · source_derived_draft · unverified_draft
### vc-transport-rbc-sugar-competition Human erythrocyte and inside-out-vesicle kinetic assays showed DHA and 3-O-methylglucose competing at both membrane faces, consistent with transport through the same GLUT1 complex. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: A later kinetic study found that sugar and oxidized vitamin C share the red-cell GLUT1 transport pathway. organism: Homo sapiens tissue_or_cell_type: Erythrocyte plasma membrane and inside-out vesicles experimental_model: Human erythrocytes, ghosts and inside-out membrane vesicles limitations: 3-O-methylglucose is a transport probe, not dietary glucose. This challenges segregated transport pools without denying vitamin C recycling. exposure: Initial-rate substrate competition and trans-acceleration assays cross_nutrient: true [sage2014] Human erythrocytes transport dehydroascorbic acid and sugars using the same transporter complex. (2014). https://pubmed.ncbi.nlm.nih.gov/24598365/ DOI: 10.1152/ajpcell.00044.2014
Complete structured claim and evidence
Where it participates (unsigned role)
Phlorizin normalization of glycemia restored adipocyte insulin-stimulated glucose transport and whole-body disposal despite persistently reduced transporter protein and mRNA.
Experimental context and source evidence
- dose
- Phlorizin sufficient to normalize blood glucose
- duration
- Chronic normalization interval
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- evidence_scope
- literature_reviewed; model-specific source-derived curation
- experimental_model
- Ninety-percent-pancreatectomized diabetic rats and isolated adipocytes
- limitations
- Restored function without restored expression points to ambient-glucose effects; it does not identify a direct phlorizin target in adipocytes.
- nutrient_topic
- Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
- organism
- Ninety-percent-pancreatectomized diabetic rats and isolated adipocytes
- plain_language
- Phlorizin normalization of glycemia restored adipocyte insulin-stimulated glucose transport and whole-body disposal despite persistently reduced transporter protein and mRNA.
- primary_references
- Normalization of blood glucose in diabetic rats with phlorizin treatment reverses insulin-resistant glucose transport in adipose cells without restoring glucose transporter gene expression. (1991). https://pubmed.ncbi.nlm.nih.gov/1991839/ DOI: 10.1172/JCI115031
- route
- In vivo treatment followed by ex-vivo cells
- tissue
- Glucose clamps, 3-O-methylglucose transport and transporter expression
Phlorizin: mechanism of action and interactions (2026-09-20) · lines 110–119
Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Ninety-percent-pancreatectomized diabetic rats and isolated adipocytes · source_derived_draft · unverified_draft
## phlorizin-adipocyte-transport-restoration Phlorizin normalization of glycemia restored adipocyte insulin-stimulated glucose transport and whole-body disposal despite persistently reduced transporter protein and mRNA. Model/species: Ninety-percent-pancreatectomized diabetic rats and isolated adipocytes Tissue/system: Glucose clamps, 3-O-methylglucose transport and transporter expression Exposure: Phlorizin sufficient to normalize blood glucose Route: In vivo treatment followed by ex-vivo cells Duration: Chronic normalization interval Limits: Restored function without restored expression points to ambient-glucose effects; it does not identify a direct phlorizin target in adipocytes. Primary reference: Normalization of blood glucose in diabetic rats with phlorizin treatment reverses insulin-resistant glucose transport in adipose cells without restoring glucose transporter gene expression. (1991). https://pubmed.ncbi.nlm.nih.gov/1991839/ DOI: 10.1172/JCI115031 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.