Component

Rat GLUT4 translocation to the cell surface

Rat GLUT4 translocation to the cell surface. Species, exposure and limitations are retained in each linked claim.

4 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. CGA increased GLUT4 delivery to the L6 plasma membrane.

    Chlorogenic acid / 5-O-caffeoylquinic acid → Rat GLUT4 translocation to the cell surface source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/chlorogenic_acid-research/22412912.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77c1ccf86d3fb56135a01d2d80b9f1eec3d657e825789f8be490fff93feb8fff", "start_char": 0, "end_char": 1896, "text_sha256": "77c1ccf86d3fb56135a01d2d80b9f1eec3d657e825789f8be490fff93feb8fff"}
    experimental_model
    L6 myotube signaling with siRNA and pharmacological tests; db/db mouse experiments
    exposure
    L6 experiments included 2 mmol/L CGA; mouse acute intervention 250 mg/kg intraperitoneally
    limitations
    Millimolar culture exposure and injected mouse doses are not dietary human exposures. Phosphorylation and abundance readouts do not by themselves prove every upstream causal step.
    nutrient_topic
    Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. · Chlorogenic acid / 5-O-caffeoylquinic acid
    organism
    Rattus norvegicus
    plain_language
    More transporter at the surface can change glucose entry.
    primary_references
    [chlorogenic_acid-p22412912] Chlorogenic acid stimulates glucose transport in skeletal muscle via AMPK activation: a contributor to the beneficial effects of coffee on diabetes. (2012). https://pubmed.ncbi.nlm.nih.gov/22412912/ DOI: 10.1371/journal.pone.0032718
    tissue_or_cell_type
    L6 skeletal-muscle myotubes

    Chlorogenic acid: metabolism, signaling and nutrient connections (2026-09-17) · lines 438–449

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · L6 myotube signaling with siRNA and pharmacological tests; db/db mouse experiments · source_derived_draft · unverified_draft

    ### chlorogenic_acid-glut4-translocation CGA increased GLUT4 delivery to the L6 plasma membrane. Condition category: normal nutrient_topic: Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: More transporter at the surface can change glucose entry. organism: Rattus norvegicus tissue_or_cell_type: L6 skeletal-muscle myotubes experimental_model: L6 myotube signaling with siRNA and pharmacological tests; db/db mouse experiments limitations: Millimolar culture exposure and injected mouse doses are not dietary human exposures. Phosphorylation and abundance readouts do not by themselves prove every upstream causal step. exposure: L6 experiments included 2 mmol/L CGA; mouse acute intervention 250 mg/kg intraperitoneally evidence_span: {"source_cache": "artifacts/chlorogenic_acid-research/22412912.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77c1ccf86d3fb56135a01d2d80b9f1eec3d657e825789f8be490fff93feb8fff", "start_char": 0, "end_char": 1896, "text_sha256": "77c1ccf86d3fb56135a01d2d80b9f1eec3d657e825789f8be490fff93feb8fff"} [chlorogenic_acid-p22412912] Chlorogenic acid stimulates glucose transport in skeletal muscle via AMPK activation: a contributor to the beneficial effects of coffee on diabetes. (2012). https://pubmed.ncbi.nlm.nih.gov/22412912/ DOI: 10.1371/journal.pone.0032718
    Complete structured claim and evidence

  2. AMPK silencing abolished chromium picolinate’s protection against impaired GLUT4 regulation in hyperinsulinemic L6 myotubes.

    Rat AMP-activated protein kinase complexes → Rat GLUT4 translocation to the cell surface source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"}
    experimental_model
    Hyperinsulinemia model with AMPK silencing
    exposure
    Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA
    limitations
    Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment.
    nutrient_topic
    Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
    organism
    Rat L6 skeletal muscle myotubes
    plain_language
    When AMPK was depleted, this transporter response to chromium picolinate was lost.
    primary_references
    [chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
    tissue_or_cell_type
    Cultured muscle plasma membrane and cortical actin
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 393–404

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hyperinsulinemia model with AMPK silencing · source_derived_draft · unverified_draft

    ### chromium-ampk-required-glut4 AMPK silencing abolished chromium picolinate’s protection against impaired GLUT4 regulation in hyperinsulinemic L6 myotubes. Condition category: machinery_impairment nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: When AMPK was depleted, this transporter response to chromium picolinate was lost. organism: Rat L6 skeletal muscle myotubes tissue_or_cell_type: Cultured muscle plasma membrane and cortical actin experimental_model: Hyperinsulinemia model with AMPK silencing limitations: Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment. exposure: Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA evidence_span: {"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"} [chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
    Complete structured claim and evidence

  3. Lipoic acid increased surface GLUT4 in L6 myotubes.

    Lipoic acid → Rat GLUT4 translocation to the cell surface source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ala-research/11375349.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "971e4224c0ff09f05d25fe64359a3c65d50f2187fd781840c55821c47d2ed111", "start_char": 0, "end_char": 1734, "text_sha256": "971e4224c0ff09f05d25fe64359a3c65d50f2187fd781840c55821c47d2ed111"}
    experimental_model
    Signaling, transporter localization and glucose-uptake assays
    exposure
    2.5 mmol/L lipoic acid; PI3K and p38 inhibitors
    limitations
    High cell-culture exposure; pharmacological inhibitors can have off-target effects; not a plasma target or patient dose.
    nutrient_topic
    Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. · Lipoic acid
    organism
    Rat
    plain_language
    More glucose transporters reached the cell surface.
    primary_references
    [ala-p11375349] The antihyperglycemic drug alpha-lipoic acid stimulates glucose uptake via both GLUT4 translocation and GLUT4 activation: potential role of p38 mitogen-activated protein kinase in GLUT4 activation. (2001). https://pubmed.ncbi.nlm.nih.gov/11375349/ DOI: 10.2337/diabetes.50.6.1464
    tissue_or_cell_type
    L6 myotubes

    Alpha-lipoic acid: cofactor assembly, redox signaling and nutrient interactions (2026-09-17) · lines 910–921

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Signaling, transporter localization and glucose-uptake assays · source_derived_draft · unverified_draft

    ### ala-myotube-glut4 Lipoic acid increased surface GLUT4 in L6 myotubes. Condition category: normal nutrient_topic: Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: More glucose transporters reached the cell surface. organism: Rat tissue_or_cell_type: L6 myotubes experimental_model: Signaling, transporter localization and glucose-uptake assays limitations: High cell-culture exposure; pharmacological inhibitors can have off-target effects; not a plasma target or patient dose. exposure: 2.5 mmol/L lipoic acid; PI3K and p38 inhibitors evidence_span: {"source_cache": "artifacts/ala-research/11375349.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "971e4224c0ff09f05d25fe64359a3c65d50f2187fd781840c55821c47d2ed111", "start_char": 0, "end_char": 1734, "text_sha256": "971e4224c0ff09f05d25fe64359a3c65d50f2187fd781840c55821c47d2ed111"} [ala-p11375349] The antihyperglycemic drug alpha-lipoic acid stimulates glucose uptake via both GLUT4 translocation and GLUT4 activation: potential role of p38 mitogen-activated protein kinase in GLUT4 activation. (2001). https://pubmed.ncbi.nlm.nih.gov/11375349/ DOI: 10.2337/diabetes.50.6.1464
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. p38 inhibitors reduced lipoic-acid-stimulated glucose uptake without blocking GLUT4 translocation in L6 myotubes.

    Rat p38 MAP kinase enzymes → Rat myotube glucose uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ala-research/11375349.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "971e4224c0ff09f05d25fe64359a3c65d50f2187fd781840c55821c47d2ed111", "start_char": 0, "end_char": 1734, "text_sha256": "971e4224c0ff09f05d25fe64359a3c65d50f2187fd781840c55821c47d2ed111"}
    experimental_model
    Signaling, transporter localization and glucose-uptake assays
    exposure
    2.5 mmol/L lipoic acid; PI3K and p38 inhibitors
    limitations
    High cell-culture exposure; pharmacological inhibitors can have off-target effects; not a plasma target or patient dose.
    nutrient_topic
    Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. · Lipoic acid
    organism
    Rat
    plain_language
    Transporter location and actual glucose movement were separable measurements.
    primary_references
    [ala-p11375349] The antihyperglycemic drug alpha-lipoic acid stimulates glucose uptake via both GLUT4 translocation and GLUT4 activation: potential role of p38 mitogen-activated protein kinase in GLUT4 activation. (2001). https://pubmed.ncbi.nlm.nih.gov/11375349/ DOI: 10.2337/diabetes.50.6.1464
    tissue_or_cell_type
    L6 myotubes

    Alpha-lipoic acid: cofactor assembly, redox signaling and nutrient interactions (2026-09-17) · lines 923–934

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Signaling, transporter localization and glucose-uptake assays · source_derived_draft · unverified_draft

    ### ala-p38-uptake-localization p38 inhibitors reduced lipoic-acid-stimulated glucose uptake without blocking GLUT4 translocation in L6 myotubes. Condition category: normal nutrient_topic: Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: Transporter location and actual glucose movement were separable measurements. organism: Rat tissue_or_cell_type: L6 myotubes experimental_model: Signaling, transporter localization and glucose-uptake assays limitations: High cell-culture exposure; pharmacological inhibitors can have off-target effects; not a plasma target or patient dose. exposure: 2.5 mmol/L lipoic acid; PI3K and p38 inhibitors evidence_span: {"source_cache": "artifacts/ala-research/11375349.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "971e4224c0ff09f05d25fe64359a3c65d50f2187fd781840c55821c47d2ed111", "start_char": 0, "end_char": 1734, "text_sha256": "971e4224c0ff09f05d25fe64359a3c65d50f2187fd781840c55821c47d2ed111"} [ala-p11375349] The antihyperglycemic drug alpha-lipoic acid stimulates glucose uptake via both GLUT4 translocation and GLUT4 activation: potential role of p38 mitogen-activated protein kinase in GLUT4 activation. (2001). https://pubmed.ncbi.nlm.nih.gov/11375349/ DOI: 10.2337/diabetes.50.6.1464
    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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