Component

Human glucose transporter 1 / SLC2A1

Human glucose transporter 1 / SLC2A1

5 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What acts on it

  1. Molecular docking proposed cucurbitacin D binding to GLUT1.

    Cucurbitacin D → Human glucose transporter 1 / SLC2A1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Computational docking within the glucose-metabolism study.
    limitations
    No transporter-binding kinetics or reconstituted transport-inhibition measurement was established by docking.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Direct transporter binding remains a prediction in this evidence record.
    primary_references
    Cucurbitacin D Reprograms Glucose Metabolic Network in Prostate Cancer. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30875788/ · DOI 10.3390/cancers11030364

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 324–330

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Computational docking within the glucose-metabolism study. · source_derived_draft · unverified_draft

    ## cucurbitacin-d-glut1-docking Direct transporter binding remains a prediction in this evidence record. Molecular docking proposed cucurbitacin D binding to GLUT1. Model: Computational docking within the glucose-metabolism study. Limitations: No transporter-binding kinetics or reconstituted transport-inhibition measurement was established by docking. Evidence access: Primary abstract Cucurbitacin D Reprograms Glucose Metabolic Network in Prostate Cancer. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30875788/ · DOI 10.3390/cancers11030364
    Complete structured claim and evidence

  2. Cucurbitacin D decreased GLUT1 expression in the prostate-cancer study; miR-132-associated changes were also reported.

    Cucurbitacin D → Human glucose transporter 1 / SLC2A1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human PC3/DU145 cells and xenograft work.
    limitations
    Expression and correlated microRNA changes do not establish a single exclusive mechanism.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Transporter abundance offers one route to altered glucose handling.
    primary_references
    Cucurbitacin D Reprograms Glucose Metabolic Network in Prostate Cancer. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30875788/ · DOI 10.3390/cancers11030364

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 316–322

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human PC3/DU145 cells and xenograft work. · source_derived_draft · unverified_draft

    ## cucurbitacin-d-glut1-expression Transporter abundance offers one route to altered glucose handling. Cucurbitacin D decreased GLUT1 expression in the prostate-cancer study; miR-132-associated changes were also reported. Model: Human PC3/DU145 cells and xenograft work. Limitations: Expression and correlated microRNA changes do not establish a single exclusive mechanism. Evidence access: Primary abstract Cucurbitacin D Reprograms Glucose Metabolic Network in Prostate Cancer. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30875788/ · DOI 10.3390/cancers11030364
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Montel-Hagen et al. reported that 5 mM glucose did not inhibit DHA accumulation in mature human erythrocytes and interpreted this as preferential DHA transport.

    D-glucose → Cellular dehydroascorbic acid uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    Human erythroid progenitors, mature RBCs and A431 stomatin transfection
    exposure
    5 mM glucose with radiolabeled DHA; room-temperature uptake time courses
    limitations
    Published interpretation challenged by kinetic analyses that distinguish transport, intracellular reduction and sugar loading.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Homo sapiens
    plain_language
    One study reported that glucose did not compete with oxidized vitamin C uptake in mature red cells.
    primary_references
    [montelhagen2008] Erythrocyte Glut1 triggers dehydroascorbic acid uptake in mammals unable to synthesize vitamin C. (2008). https://pubmed.ncbi.nlm.nih.gov/18358815/ DOI: 10.1016/j.cell.2008.01.042
    tissue_or_cell_type
    Mature erythrocytes

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 520–531

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human erythroid progenitors, mature RBCs and A431 stomatin transfection · source_derived_draft · unverified_draft

    ### vc-transport-rbc-glucose-noncompetition Montel-Hagen et al. reported that 5 mM glucose did not inhibit DHA accumulation in mature human erythrocytes and interpreted this as preferential DHA transport. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: One study reported that glucose did not compete with oxidized vitamin C uptake in mature red cells. organism: Homo sapiens tissue_or_cell_type: Mature erythrocytes experimental_model: Human erythroid progenitors, mature RBCs and A431 stomatin transfection limitations: Published interpretation challenged by kinetic analyses that distinguish transport, intracellular reduction and sugar loading. exposure: 5 mM glucose with radiolabeled DHA; room-temperature uptake time courses cross_nutrient: true [montelhagen2008] Erythrocyte Glut1 triggers dehydroascorbic acid uptake in mammals unable to synthesize vitamin C. (2008). https://pubmed.ncbi.nlm.nih.gov/18358815/ DOI: 10.1016/j.cell.2008.01.042
    Complete structured claim and evidence

  2. 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.

    3-O-Methyl-D-glucose → Dehydroascorbic acid source_derived_draftungraded
    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

  3. Stomatin transfection increased DHA uptake in human A431 cells while GLUT1 abundance was unchanged; GLUT1 knockdown reduced uptake.

    Human stomatin / STOM → Cellular dehydroascorbic acid uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human erythroid progenitors, mature RBCs and A431 stomatin transfection
    exposure
    Stomatin transfection; 30- and 300-second uptake assays
    limitations
    Cancer cell line; preferential-transport interpretation is disputed by later erythrocyte kinetics.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Homo sapiens
    plain_language
    Stomatin changed oxidized vitamin C uptake without simply adding more GLUT1 protein.
    primary_references
    [montelhagen2008] Erythrocyte Glut1 triggers dehydroascorbic acid uptake in mammals unable to synthesize vitamin C. (2008). https://pubmed.ncbi.nlm.nih.gov/18358815/ DOI: 10.1016/j.cell.2008.01.042
    tissue_or_cell_type
    A431 cells

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 507–518

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human erythroid progenitors, mature RBCs and A431 stomatin transfection · source_derived_draft · unverified_draft

    ### vc-transport-stomatin-dha Stomatin transfection increased DHA uptake in human A431 cells while GLUT1 abundance was unchanged; GLUT1 knockdown reduced uptake. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Stomatin changed oxidized vitamin C uptake without simply adding more GLUT1 protein. organism: Homo sapiens tissue_or_cell_type: A431 cells experimental_model: Human erythroid progenitors, mature RBCs and A431 stomatin transfection limitations: Cancer cell line; preferential-transport interpretation is disputed by later erythrocyte kinetics. exposure: Stomatin transfection; 30- and 300-second uptake assays cross_nutrient: false [montelhagen2008] Erythrocyte Glut1 triggers dehydroascorbic acid uptake in mammals unable to synthesize vitamin C. (2008). https://pubmed.ncbi.nlm.nih.gov/18358815/ DOI: 10.1016/j.cell.2008.01.042
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards