Component

Rat AMP-activated protein kinase complexes

Rat AMP-activated protein kinase complexes. Species, exposure and limitations are retained in each linked claim.

10 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.

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 it acts on

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

    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
  2. AMPK silencing abolished chromium picolinate’s protection against impaired glucose transport in the same L6 model.

    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
    The glucose-uptake benefit also depended on AMPK in this experiment.
    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 406–417

    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-uptake AMPK silencing abolished chromium picolinate’s protection against impaired glucose transport in the same L6 model. Condition category: machinery_impairment nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The glucose-uptake benefit also depended on AMPK in this experiment. 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

What acts on it

  1. CGA increased AMPK phosphorylation and measured AMPK activity in L6 myotubes.

    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
    A cellular energy-sensing pathway responded in cultured rat muscle.
    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 412–423

    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-ampk-activation CGA increased AMPK phosphorylation and measured AMPK activity in L6 myotubes. Condition category: normal nutrient_topic: Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: A cellular energy-sensing pathway responded in cultured rat muscle. 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. Mangiferin increased AMPK phosphorylation in L6 myotubes.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"}
    experimental_model
    Normal and insulin-resistant L6 myotube comparison
    exposure
    Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin
    limitations
    Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering.
    nutrient_topic
    Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
    organism
    Rattus norvegicus
    plain_language
    The energy-sensing pathway responded in this cell model.
    primary_references
    [mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
    tissue_or_cell_type
    L6 myotubes

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 379–390

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Normal and insulin-resistant L6 myotube comparison · source_derived_draft · unverified_draft

    ### mangiferin-mangiferin-ampk Mangiferin increased AMPK phosphorylation in L6 myotubes. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The energy-sensing pathway responded in this cell model. organism: Rattus norvegicus tissue_or_cell_type: L6 myotubes experimental_model: Normal and insulin-resistant L6 myotube comparison limitations: Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering. exposure: Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin evidence_span: {"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"} [mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
    Complete structured claim and evidence
  3. Norathyriol increased AMPK phosphorylation in L6 myotubes.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"}
    experimental_model
    Normal and insulin-resistant L6 myotube comparison
    exposure
    Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin
    limitations
    Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering.
    nutrient_topic
    Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
    organism
    Rattus norvegicus
    plain_language
    The energy-sensing pathway responded in this cell model.
    primary_references
    [mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
    tissue_or_cell_type
    L6 myotubes

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 392–403

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Normal and insulin-resistant L6 myotube comparison · source_derived_draft · unverified_draft

    ### mangiferin-norathyriol-ampk Norathyriol increased AMPK phosphorylation in L6 myotubes. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The energy-sensing pathway responded in this cell model. organism: Rattus norvegicus tissue_or_cell_type: L6 myotubes experimental_model: Normal and insulin-resistant L6 myotube comparison limitations: Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering. exposure: Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin evidence_span: {"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"} [mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
    Complete structured claim and evidence
  4. Chromium picolinate increased AMPK signaling in L6 myotubes without enhancing the proximal insulin-signaling responses measured in that experiment.

    Experimental context and source evidence
    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
    The response involved the cell’s energy-sensing pathway rather than a measured increase in proximal insulin signaling.
    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

    Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 354–365

    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-response Chromium picolinate increased AMPK signaling in L6 myotubes without enhancing the proximal insulin-signaling responses measured in that experiment. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response involved the cell’s energy-sensing pathway rather than a measured increase in proximal insulin signaling. 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
  5. Berberine increased AMPK phosphorylation in L6 myotubes.

    Berberine → Rat AMP-activated protein kinase complexes source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/berberine-research/18285556.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cd721d78117d554be4fdb0403ac792f6723cf59cfd3679106607e8f17eafc257", "start_char": 0, "end_char": 1735, "text_sha256": "cd721d78117d554be4fdb0403ac792f6723cf59cfd3679106607e8f17eafc257"}
    experimental_model
    Cell respiration, isolated mitochondria and kinase perturbation
    exposure
    Berberine concentration-response; kinase deletion/inhibition
    limitations
    Functional respiratory inhibition does not by itself establish direct binding to complex I or improved mitochondrial health. Preclinical exposure, not human efficacy.
    nutrient_topic
    Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
    organism
    Rat L6 myotubes, muscle mitochondria and LKB1-deficient cells
    plain_language
    AMPK responds to the altered cellular energy state in this model.
    primary_references
    [berberine-p18285556] Berberine and its more biologically available derivative, dihydroberberine, inhibit mitochondrial respiratory complex I: a mechanism for the action of berberine to activate AMP-activated protein kinase and improve insulin action. (2008). https://pubmed.ncbi.nlm.nih.gov/18285556/ DOI: 10.2337/db07-1552
    tissue_or_cell_type
    Respiratory complex I and AMPK

    Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 337–348

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell respiration, isolated mitochondria and kinase perturbation · source_derived_draft · unverified_draft

    ### berberine-ampk Berberine increased AMPK phosphorylation in L6 myotubes. Condition category: normal nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: AMPK responds to the altered cellular energy state in this model. organism: Rat L6 myotubes, muscle mitochondria and LKB1-deficient cells tissue_or_cell_type: Respiratory complex I and AMPK experimental_model: Cell respiration, isolated mitochondria and kinase perturbation limitations: Functional respiratory inhibition does not by itself establish direct binding to complex I or improved mitochondrial health. Preclinical exposure, not human efficacy. exposure: Berberine concentration-response; kinase deletion/inhibition evidence_span: {"source_cache": "artifacts/berberine-research/18285556.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cd721d78117d554be4fdb0403ac792f6723cf59cfd3679106607e8f17eafc257", "start_char": 0, "end_char": 1735, "text_sha256": "cd721d78117d554be4fdb0403ac792f6723cf59cfd3679106607e8f17eafc257"} [berberine-p18285556] Berberine and its more biologically available derivative, dihydroberberine, inhibit mitochondrial respiratory complex I: a mechanism for the action of berberine to activate AMP-activated protein kinase and improve insulin action. (2008). https://pubmed.ncbi.nlm.nih.gov/18285556/ DOI: 10.2337/db07-1552
    Complete structured claim and evidence
  6. Adding (S)-6-gingerol increased AMPK alpha Thr172 phosphorylation in rat L6 cells, with CaMKK-associated signaling.

    Experimental context and source evidence
    dose
    (S)-6-Gingerol; dose-response, exact range not in accessed abstract
    duration
    Time-dependent response; exact times not in accessed abstract
    evidence_access
    Primary PubMed abstract.
    evidence_scope
    literature_reviewed; model-specific source-derived curation, not universally established human effects
    experimental_model
    Rat L6 skeletal muscle myotubes
    limitations
    Calcium/CaMKK-associated signaling does not demonstrate dietary calcium depletion or calcium-supplement synergy; no human glycemic outcome was tested. The accessed abstract does not identify a CaMKK isoform or establish genetic necessity.
    nutrient_topic
    Gingerols collection; each molecular form and experimental preparation remains explicit. · Gingerols
    organism
    Rat L6 skeletal muscle myotubes
    plain_language
    Adding (S)-6-gingerol increased AMPK alpha Thr172 phosphorylation in rat L6 cells, with CaMKK-associated signaling.
    primary_references
    (S)-[6]-Gingerol enhances glucose uptake in L6 myotubes by activation of AMPK in response to [Ca2+]i. (2013). https://pubmed.ncbi.nlm.nih.gov/23958199/ DOI: 10.18433/j34g7p
    route
    In vitro addition
    tissue
    Skeletal muscle cell model

    Gingerols: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 162–171

    Original AI-assisted curation of thirteen primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Rat L6 skeletal muscle myotubes · source_derived_draft · unverified_draft

    ## gingerols-6-l6-ampk Adding (S)-6-gingerol increased AMPK alpha Thr172 phosphorylation in rat L6 cells, with CaMKK-associated signaling. Model/species: Rat L6 skeletal muscle myotubes Tissue: Skeletal muscle cell model Exposure: (S)-6-Gingerol; dose-response, exact range not in accessed abstract Route: In vitro addition Duration: Time-dependent response; exact times not in accessed abstract Limits: Calcium/CaMKK-associated signaling does not demonstrate dietary calcium depletion or calcium-supplement synergy; no human glycemic outcome was tested. The accessed abstract does not identify a CaMKK isoform or establish genetic necessity. Primary reference: (S)-[6]-Gingerol enhances glucose uptake in L6 myotubes by activation of AMPK in response to [Ca2+]i. (2013). https://pubmed.ncbi.nlm.nih.gov/23958199/ DOI: 10.18433/j34g7p Access: Primary PubMed abstract.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. AMPK alpha1/alpha2 knockdown abrogated CGA-stimulated glucose transport.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    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
    The response depends on functioning machinery in this model.
    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 myotubes
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Chlorogenic acid: metabolism, signaling and nutrient connections (2026-09-17) · lines 490–501

    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-ampk-loss AMPK alpha1/alpha2 knockdown abrogated CGA-stimulated glucose transport. Condition category: machinery_impairment nutrient_topic: Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response depends on functioning machinery in this model. organism: Rattus norvegicus tissue_or_cell_type: L6 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. Adding (S)-6-gingerol increased glucose uptake in rat L6 myotubes.

    6-Gingerol → Rat myotube glucose uptake source_derived_draftungraded
    Experimental context and source evidence
    dose
    (S)-6-Gingerol; dose-response, exact range not in accessed abstract
    duration
    Time-dependent response; exact times not in accessed abstract
    evidence_access
    Primary PubMed abstract.
    evidence_scope
    literature_reviewed; model-specific source-derived curation, not universally established human effects
    experimental_model
    Rat L6 skeletal muscle myotubes
    limitations
    Calcium/CaMKK-associated signaling does not demonstrate dietary calcium depletion or calcium-supplement synergy; no human glycemic outcome was tested.
    nutrient_topic
    Gingerols collection; each molecular form and experimental preparation remains explicit. · Gingerols
    organism
    Rat L6 skeletal muscle myotubes
    plain_language
    Adding (S)-6-gingerol increased glucose uptake in rat L6 myotubes.
    primary_references
    (S)-[6]-Gingerol enhances glucose uptake in L6 myotubes by activation of AMPK in response to [Ca2+]i. (2013). https://pubmed.ncbi.nlm.nih.gov/23958199/ DOI: 10.18433/j34g7p
    route
    In vitro addition
    tissue
    Skeletal muscle cell model

    Gingerols: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 173–182

    Original AI-assisted curation of thirteen primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Rat L6 skeletal muscle myotubes · source_derived_draft · unverified_draft

    ## gingerols-6-l6-glucose Adding (S)-6-gingerol increased glucose uptake in rat L6 myotubes. Model/species: Rat L6 skeletal muscle myotubes Tissue: Skeletal muscle cell model Exposure: (S)-6-Gingerol; dose-response, exact range not in accessed abstract Route: In vitro addition Duration: Time-dependent response; exact times not in accessed abstract Limits: Calcium/CaMKK-associated signaling does not demonstrate dietary calcium depletion or calcium-supplement synergy; no human glycemic outcome was tested. Primary reference: (S)-[6]-Gingerol enhances glucose uptake in L6 myotubes by activation of AMPK in response to [Ca2+]i. (2013). https://pubmed.ncbi.nlm.nih.gov/23958199/ DOI: 10.18433/j34g7p Access: Primary PubMed abstract.
    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