Component

Mouse glucose transporter 4 / Slc2a4

Mouse glucose transporter 4 / Slc2a4. Species, exposure and limitations are retained in each linked claim.

7 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. Chromium co-treatment increased GLUT4 levels relative to the iron-only condition, alongside higher PI3K and Akt phosphorylation ratios.

    Chromium(III) picolinate / CrPic → Mouse glucose transporter 4 / Slc2a4 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/chromium-research/37156991.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda", "start_char": 0, "end_char": 1621, "text_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda"}
    experimental_model
    C2C12 cell experiments with supporting database pathway analysis
    exposure
    Chromium picolinate, ferric ammonium citrate and combination
    limitations
    Pathway databases generate hypotheses. Co-changing ROS and signaling measurements do not alone establish a unique causal sequence; no human iron-overload treatment was tested.
    nutrient_topic
    Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
    organism
    Mouse C2C12 skeletal-muscle cells
    plain_language
    The glucose transporter and measured signaling steps were less suppressed.
    primary_references
    [chromium-p37156991] Antagonizing Effects of Chromium Against Iron-Decreased Glucose Uptake by Regulating ROS-Mediated PI3K/Akt/GLUT4 Signaling Pathway in C2C12. (2024). https://pubmed.ncbi.nlm.nih.gov/37156991/ DOI: 10.1007/s12011-023-03695-z
    tissue_or_cell_type
    Cellular glucose uptake, ROS assays and signaling proteins

    Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 796–807

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · C2C12 cell experiments with supporting database pathway analysis · source_derived_draft · unverified_draft

    ### chromium-iron-cell-glut4 Chromium co-treatment increased GLUT4 levels relative to the iron-only condition, alongside higher PI3K and Akt phosphorylation ratios. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The glucose transporter and measured signaling steps were less suppressed. organism: Mouse C2C12 skeletal-muscle cells tissue_or_cell_type: Cellular glucose uptake, ROS assays and signaling proteins experimental_model: C2C12 cell experiments with supporting database pathway analysis limitations: Pathway databases generate hypotheses. Co-changing ROS and signaling measurements do not alone establish a unique causal sequence; no human iron-overload treatment was tested. exposure: Chromium picolinate, ferric ammonium citrate and combination evidence_span: {"source_cache": "artifacts/chromium-research/37156991.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda", "start_char": 0, "end_char": 1621, "text_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda"} [chromium-p37156991] Antagonizing Effects of Chromium Against Iron-Decreased Glucose Uptake by Regulating ROS-Mediated PI3K/Akt/GLUT4 Signaling Pathway in C2C12. (2024). https://pubmed.ncbi.nlm.nih.gov/37156991/ DOI: 10.1007/s12011-023-03695-z
    Complete structured claim and evidence

  2. During mouse 3T3-L1 differentiation, fisetin reduced GLUT4 expression and glucose uptake.

    Fisetin → Mouse glucose transporter 4 / Slc2a4 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Differentiating mouse adipocytes.
    limitations
    This is not evidence that fisetin improves glucose uptake in human muscle.
    nutrient_topic
    Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin
    plain_language
    Less glucose entry reduced lipid accumulation in this model.
    primary_references
    Fisetin Suppresses Lipid Accumulation in Mouse Adipocytic 3T3-L1 Cells by Repressing GLUT4-Mediated Glucose Uptake through Inhibition of mTOR-C/EBPα Signaling. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25945786/ · DOI 10.1021/acs.jafc.5b00821

    Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 296–302

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Differentiating mouse adipocytes. · source_derived_draft · unverified_draft

    ## fisetin-adipocyte-glut4 Less glucose entry reduced lipid accumulation in this model. During mouse 3T3-L1 differentiation, fisetin reduced GLUT4 expression and glucose uptake. Model: Differentiating mouse adipocytes. Limitations: This is not evidence that fisetin improves glucose uptake in human muscle. Evidence access: Primary abstract Fisetin Suppresses Lipid Accumulation in Mouse Adipocytic 3T3-L1 Cells by Repressing GLUT4-Mediated Glucose Uptake through Inhibition of mTOR-C/EBPα Signaling. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25945786/ · DOI 10.1021/acs.jafc.5b00821
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. In mouse 3T3-L1 cells, luteolin suppressed adipogenesis and several PPAR gamma targets while increasing GLUT4 expression.

    Luteolin / 3′,4′,5,7-tetrahydroxyflavone → Mouse peroxisome proliferator-activated receptor gamma / Pparg source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse adipocyte differentiation and gene expression.
    limitations
    GLUT4 expression is not proof of increased glucose uptake in humans.
    nutrient_topic
    Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
    plain_language
    One receptor can produce different responses at different genes.
    primary_references
    Mode of peroxisome proliferator-activated receptor γ activation by luteolin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22391103/ · DOI 10.1124/mol.111.076216

    Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 372–378

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse adipocyte differentiation and gene expression. · source_derived_draft · unverified_draft

    ## luteolin-pparg-gene-specific One receptor can produce different responses at different genes. In mouse 3T3-L1 cells, luteolin suppressed adipogenesis and several PPAR gamma targets while increasing GLUT4 expression. Model: Mouse adipocyte differentiation and gene expression. Limitations: GLUT4 expression is not proof of increased glucose uptake in humans. Evidence access: Primary abstract Mode of peroxisome proliferator-activated receptor γ activation by luteolin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22391103/ · DOI 10.1124/mol.111.076216
    Complete structured claim and evidence

  2. The tested chloride form mobilized GLUT4-containing vesicles toward the cell surface; insulin promoted their incorporation into the plasma membrane.

    Chromium(III) chloride → Mouse GLUT4 movement toward or into the cell surface source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"}
    experimental_model
    GLUT4 trafficking, glucose uptake and cholesterol add-back experiments
    exposure
    Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation
    limitations
    Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found.
    nutrient_topic
    Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
    organism
    Mouse 3T3-L1 adipocytes
    plain_language
    Chromium exposure moved glucose transporters closer to the surface, but insulin was still needed for the functional response.
    primary_references
    [chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
    tissue_or_cell_type
    Cultured adipocyte plasma membrane

    Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 315–326

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GLUT4 trafficking, glucose uptake and cholesterol add-back experiments · source_derived_draft · unverified_draft

    ### chromium-chloride-glut4 The tested chloride form mobilized GLUT4-containing vesicles toward the cell surface; insulin promoted their incorporation into the plasma membrane. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Chromium exposure moved glucose transporters closer to the surface, but insulin was still needed for the functional response. organism: Mouse 3T3-L1 adipocytes tissue_or_cell_type: Cultured adipocyte plasma membrane experimental_model: GLUT4 trafficking, glucose uptake and cholesterol add-back experiments limitations: Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found. exposure: Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation evidence_span: {"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"} [chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
    Complete structured claim and evidence

  3. Chromium-associated membrane-cholesterol reduction accompanied enhanced insulin-stimulated glucose uptake, and cholesterol add-back prevented the trafficking and uptake benefit.

    Chromium(III) picolinate / CrPic → Insulin-stimulated glucose uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"}
    experimental_model
    GLUT4 trafficking, glucose uptake and cholesterol add-back experiments
    exposure
    Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation
    limitations
    Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found.
    nutrient_topic
    Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
    organism
    Mouse 3T3-L1 adipocytes
    plain_language
    Putting cholesterol back into the membrane removed the effect, supporting a membrane-dependent mechanism.
    primary_references
    [chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
    tissue_or_cell_type
    Cultured adipocyte plasma membrane

    Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 328–339

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GLUT4 trafficking, glucose uptake and cholesterol add-back experiments · source_derived_draft · unverified_draft

    ### chromium-cholesterol-dependent-uptake Chromium-associated membrane-cholesterol reduction accompanied enhanced insulin-stimulated glucose uptake, and cholesterol add-back prevented the trafficking and uptake benefit. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Putting cholesterol back into the membrane removed the effect, supporting a membrane-dependent mechanism. organism: Mouse 3T3-L1 adipocytes tissue_or_cell_type: Cultured adipocyte plasma membrane experimental_model: GLUT4 trafficking, glucose uptake and cholesterol add-back experiments limitations: Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found. exposure: Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation evidence_span: {"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"} [chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
    Complete structured claim and evidence

  4. The tested picolinate form mobilized GLUT4-containing vesicles toward the cell surface; insulin promoted their incorporation into the plasma membrane.

    Chromium(III) picolinate / CrPic → Mouse GLUT4 movement toward or into the cell surface source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"}
    experimental_model
    GLUT4 trafficking, glucose uptake and cholesterol add-back experiments
    exposure
    Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation
    limitations
    Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found.
    nutrient_topic
    Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
    organism
    Mouse 3T3-L1 adipocytes
    plain_language
    Chromium exposure moved glucose transporters closer to the surface, but insulin was still needed for the functional response.
    primary_references
    [chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
    tissue_or_cell_type
    Cultured adipocyte plasma membrane

    Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 302–313

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GLUT4 trafficking, glucose uptake and cholesterol add-back experiments · source_derived_draft · unverified_draft

    ### chromium-picolinate-glut4 The tested picolinate form mobilized GLUT4-containing vesicles toward the cell surface; insulin promoted their incorporation into the plasma membrane. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Chromium exposure moved glucose transporters closer to the surface, but insulin was still needed for the functional response. organism: Mouse 3T3-L1 adipocytes tissue_or_cell_type: Cultured adipocyte plasma membrane experimental_model: GLUT4 trafficking, glucose uptake and cholesterol add-back experiments limitations: Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found. exposure: Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation evidence_span: {"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"} [chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
    Complete structured claim and evidence

  5. Fisetin reduced C/EBP-alpha occupancy at the GLUT4 promoter in mouse 3T3-L1 cells, alongside reduced mTOR/S6K signaling.

    Fisetin → Mouse C/EBP alpha / Cebpa source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Chromatin immunoprecipitation; comparison with rapamycin.
    limitations
    Association and phenocopy do not resolve every direct target.
    nutrient_topic
    Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin
    plain_language
    A transcriptional step links signaling to glucose transport.
    primary_references
    Fisetin Suppresses Lipid Accumulation in Mouse Adipocytic 3T3-L1 Cells by Repressing GLUT4-Mediated Glucose Uptake through Inhibition of mTOR-C/EBPα Signaling. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25945786/ · DOI 10.1021/acs.jafc.5b00821

    Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 304–310

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Chromatin immunoprecipitation; comparison with rapamycin. · source_derived_draft · unverified_draft

    ## fisetin-adipocyte-promoter A transcriptional step links signaling to glucose transport. Fisetin reduced C/EBP-alpha occupancy at the GLUT4 promoter in mouse 3T3-L1 cells, alongside reduced mTOR/S6K signaling. Model: Chromatin immunoprecipitation; comparison with rapamycin. Limitations: Association and phenocopy do not resolve every direct target. Evidence access: Primary abstract Fisetin Suppresses Lipid Accumulation in Mouse Adipocytic 3T3-L1 Cells by Repressing GLUT4-Mediated Glucose Uptake through Inhibition of mTOR-C/EBPα Signaling. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25945786/ · DOI 10.1021/acs.jafc.5b00821
    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.

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