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Study · Animal study (in vivo) · mouse · 2018

6 results

The AMPK agonist 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), but not metformin, prevents inflammation-associated cachectic muscle wasting.

Hall DT, Griss T, Ma JF, Sanchez BJ, Sadek J, Tremblay AMK, Mubaid S, Omer A, Ford RJ, Bedard N, Pause A, Wing SS and 4 more

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Di Marco S, Steinberg GR, Jones RG, Gallouzi IE

EMBO molecular medicine1 Jul 2018Cited by 78 (Europe PMC)

PMID29844217 (opens in a new tab)PMCIDPMC6034131 (opens in a new tab)DOI10.15252/emmm.201708307 (opens in a new tab)PepBankPUB-29844217
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Summary

Activation of AMPK has been associated with pro-atrophic signaling in muscle. However, AMPK also has anti-inflammatory effects, suggesting that in cachexia, a syndrome of inflammatory-driven muscle wasting, AMPK activation could be beneficial. Here we show that the AMPK agonist AICAR suppresses IFNγ/TNFα-induced atrophy, while the mitochondrial inhibitor metformin does not. IFNγ/TNFα impair mitochondrial oxidative respiration in myotubes and promote a metabolic shift to aerobic glycolysis, similarly to metformin. In contrast, AICAR partially restored metabolic function. The effects of AICAR were prevented by the AMPK inhibitor Compound C and were reproduced with A-769662, a specific AMPK activator. AICAR and A-769662 co-treatment was found to be synergistic, suggesting that the anti-cachectic effects of these drugs are mediated through AMPK activation. AICAR spared muscle mass in mouse models of cancer and LPS induced atrophy. Together, our findings suggest a dual function for AMPK during inflammation-driven atrophy, wherein it can play a protective role when activated exogenously early in disease progression, but may contribute to anabolic suppression and atrophy when activated later through mitochondrial dysfunction and subsequent metabolic stress.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study6

4 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice with cancer-induced atrophy, AICAR spared muscle mass.

    In plain wordsIn mice with cancer-induced muscle wasting, AICAR preserved muscle mass.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseMuscle mass in cancer
    Study

    mousen: not reported in source

    Cancer-induced atrophy
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR spared muscle mass in mouse models of cancer and LPS induced atrophy.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with LPS-induced atrophy, AICAR spared muscle mass.

    In plain wordsIn mice with LPS-induced muscle wasting, AICAR preserved muscle mass.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseMuscle mass after LPS
    Study

    mousen: not reported in source

    LPS-induced atrophy
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR spared muscle mass in mouse models of cancer and LPS induced atrophy.
  3. 03LabIn vitro (cells)Efficacy outcome

    In myotubes, AICAR suppressed IFNγ/TNFα-induced atrophy, whereas metformin did not.

    In plain wordsIn cells, AICAR reduced inflammation-induced muscle atrophy, whereas metformin did not.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseMyotube atrophy
    Study

    n: not reported in source

    IFNγ/TNFα-treated myotubes
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we show that the AMPK agonist AICAR suppresses IFNγ/TNFα-induced atrophy, while the mitochondrial inhibitor metformin does not.
    1 context sentence
    Summary · context
    IFNγ/TNFα impair mitochondrial oxidative respiration in myotubes and promote a metabolic shift to aerobic glycolysis, similarly to metformin.
  4. 04LabIn vitro (cells)Efficacy outcome

    In IFNγ/TNFα-treated myotubes, AICAR partially restored metabolic function.

    In plain wordsIn cells exposed to inflammatory cytokines, AICAR partially restored metabolic function.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseMetabolic function
    Study

    n: not reported in source

    IFNγ/TNFα-treated myotubes
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In contrast, AICAR partially restored metabolic function.
    1 context sentence
    Summary · context
    IFNγ/TNFα impair mitochondrial oxidative respiration in myotubes and promote a metabolic shift to aerobic glycolysis, similarly to metformin.

Studies that did not test the peptide alone2

In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking AICAR (acadesine).

  1. 05LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In myotubes, Compound C prevented the effects of AICAR.

    In plain wordsIn cells, the AMPK inhibitor Compound C prevented the effects of AICAR.

    Peptide
    AICAR (acadesine)
    Outcome
    Not applicableBlockade by Compound C
    Study

    n: not reported in source

    IFNγ/TNFα-treated myotubes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    The effects of AICAR were prevented by the AMPK inhibitor Compound C and were reproduced with A-769662, a specific AMPK activator.

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

  2. 06LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Efficacy outcome

    In myotubes, combined AICAR and A-769662 treatment showed synergistic anti-cachectic effects.

    In plain wordsIn cells, AICAR combined with A-769662 showed synergistic effects against muscle wasting.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseAnti-cachectic synergy
    Study

    n: not reported in source

    IFNγ/TNFα-treated myotubes
    Outcome group
    Muscle injury and repair · Musculoskeletal

    Source sentences

    Summary
    AICAR and A-769662 co-treatment was found to be synergistic, suggesting that the anti-cachectic effects of these drugs are mediated through AMPK activation.

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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