Component

Mouse AMPK complexes

Context-specific entity; species, compartment and exposure are stated on each claim.

6 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. Intracellular calcium chelation with BAPTA-AM reduced AMPK and ACC phosphorylation induced by 50 micromolar resveratrol in mouse C2C12 myotubes.

    BAPTA-AM intracellular calcium chelator → Mouse AMPK complexes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Pharmacological intracellular calcium buffering.
    limitations
    This is not a dietary calcium-deficiency threshold.
    nutrient_topic
    Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol
    plain_language
    Removing available signaling calcium weakened the response.
    primary_references
    Resveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterases. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22304913/ · DOI 10.1016/j.cell.2012.01.017
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 254–260

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Pharmacological intracellular calcium buffering. · source_derived_draft · unverified_draft

    ## resveratrol-calcium-chelation Removing available signaling calcium weakened the response. Intracellular calcium chelation with BAPTA-AM reduced AMPK and ACC phosphorylation induced by 50 micromolar resveratrol in mouse C2C12 myotubes. Model: Pharmacological intracellular calcium buffering. Limitations: This is not a dietary calcium-deficiency threshold. Evidence access: Primary full text Resveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterases. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22304913/ · DOI 10.1016/j.cell.2012.01.017
    Complete structured claim and evidence

  2. STO609 reduced the mouse C2C12 AMPK response to 50 micromolar resveratrol but not to 300 micromolar.

    Mouse CaMKK beta / Camkk2 → Mouse AMPK complexes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Pharmacological CaMKK inhibition; two resveratrol concentrations.
    limitations
    Inhibitor specificity limits isoform-level certainty.
    nutrient_topic
    Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol
    plain_language
    Higher exposure can bypass the calcium-dependent kinase route.
    primary_references
    Resveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterases. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22304913/ · DOI 10.1016/j.cell.2012.01.017
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 262–268

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Pharmacological CaMKK inhibition; two resveratrol concentrations. · source_derived_draft · unverified_draft

    ## resveratrol-camkk-block Higher exposure can bypass the calcium-dependent kinase route. STO609 reduced the mouse C2C12 AMPK response to 50 micromolar resveratrol but not to 300 micromolar. Model: Pharmacological CaMKK inhibition; two resveratrol concentrations. Limitations: Inhibitor specificity limits isoform-level certainty. Evidence access: Primary full text Resveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterases. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22304913/ · DOI 10.1016/j.cell.2012.01.017
    Complete structured claim and evidence

  3. In mouse C2C12 cells, 25 micromolar resveratrol activated AMPK in a Sirt1-dependent manner; at 50 micromolar, activation could occur independently of Sirt1.

    Resveratrol → Mouse AMPK complexes source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse muscle-cell dose comparison.
    limitations
    Neither concentration is a demonstrated human muscle exposure.
    nutrient_topic
    Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol
    plain_language
    The route to the same signaling node changes with exposure.
    primary_references
    SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22560220/ · DOI 10.1016/j.cmet.2012.04.003

    Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 182–188

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse muscle-cell dose comparison. · source_derived_draft · unverified_draft

    ## resveratrol-mouse-ampk-dose The route to the same signaling node changes with exposure. In mouse C2C12 cells, 25 micromolar resveratrol activated AMPK in a Sirt1-dependent manner; at 50 micromolar, activation could occur independently of Sirt1. Model: Mouse muscle-cell dose comparison. Limitations: Neither concentration is a demonstrated human muscle exposure. Evidence access: Primary full text SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22560220/ · DOI 10.1016/j.cmet.2012.04.003
    Complete structured claim and evidence

  4. Ryanodine prevented resveratrol-induced AMPK/ACC phosphorylation in mouse C2C12 myotubes, supporting a ryanodine-receptor calcium-release route.

    Mouse ryanodine receptor 2 / Ryr2 → Mouse AMPK complexes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Pharmacological channel inhibition.
    limitations
    Does not establish direct resveratrol binding to Ryr2.
    nutrient_topic
    Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol
    plain_language
    Stored calcium release connects to the energy-sensing kinase.
    primary_references
    Resveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterases. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22304913/ · DOI 10.1016/j.cell.2012.01.017
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 278–284

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

    ## resveratrol-ryr-block Stored calcium release connects to the energy-sensing kinase. Ryanodine prevented resveratrol-induced AMPK/ACC phosphorylation in mouse C2C12 myotubes, supporting a ryanodine-receptor calcium-release route. Model: Pharmacological channel inhibition. Limitations: Does not establish direct resveratrol binding to Ryr2. Evidence access: Primary full text Resveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterases. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22304913/ · DOI 10.1016/j.cell.2012.01.017
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Adult-induced Sirt1 deletion prevented resveratrol-associated improvements in mouse skeletal-muscle mitochondrial function at both tested dietary doses.

    Mouse sirtuin 1 / Sirt1 → Resveratrol-associated mouse muscle mitochondrial improvement source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    High-fat-fed mice receiving approximately 25–30 or 215–230 mg/kg/day.
    limitations
    Adult knockout, tissue context and high-fat diet matter; not a human niacin-deficiency experiment.
    nutrient_topic
    Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol
    plain_language
    A response can require intact machinery even if upstream signals still change.
    primary_references
    SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22560220/ · DOI 10.1016/j.cmet.2012.04.003
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 174–180

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · High-fat-fed mice receiving approximately 25–30 or 215–230 mg/kg/day. · source_derived_draft · unverified_draft

    ## resveratrol-mouse-sirt1-loss A response can require intact machinery even if upstream signals still change. Adult-induced Sirt1 deletion prevented resveratrol-associated improvements in mouse skeletal-muscle mitochondrial function at both tested dietary doses. Model: High-fat-fed mice receiving approximately 25–30 or 215–230 mg/kg/day. Limitations: Adult knockout, tissue context and high-fat diet matter; not a human niacin-deficiency experiment. Evidence access: Primary full text SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22560220/ · DOI 10.1016/j.cmet.2012.04.003
    Complete structured claim and evidence

  2. The PLC inhibitor U73122 reduced the intracellular calcium rise and AMPK/ACC phosphorylation after resveratrol in mouse C2C12 cells.

    U73122, pharmacological PLC inhibitor → Resveratrol-induced calcium increase in mouse C2C12 cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    50 micromolar resveratrol cell experiments.
    limitations
    Supports PLC involvement; this inhibitor alone does not isolate PLC-epsilon.
    nutrient_topic
    Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol
    plain_language
    A phospholipase-linked step lies upstream of calcium signaling.
    primary_references
    Resveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterases. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22304913/ · DOI 10.1016/j.cell.2012.01.017
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 270–276

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 50 micromolar resveratrol cell experiments. · source_derived_draft · unverified_draft

    ## resveratrol-plc-calcium A phospholipase-linked step lies upstream of calcium signaling. The PLC inhibitor U73122 reduced the intracellular calcium rise and AMPK/ACC phosphorylation after resveratrol in mouse C2C12 cells. Model: 50 micromolar resveratrol cell experiments. Limitations: Supports PLC involvement; this inhibitor alone does not isolate PLC-epsilon. Evidence access: Primary full text Resveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterases. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22304913/ · DOI 10.1016/j.cell.2012.01.017
    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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