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Study · Not a test of the peptide alone · 2010

2 results

Whole body deletion of AMP-activated protein kinase {beta}2 reduces muscle AMPK activity and exercise capacity.

Steinberg GR, O'Neill HM, Dzamko NL, Galic S, Naim T, Koopman R, Jørgensen SB, Honeyman J, Hewitt K, Chen ZP, Schertzer JD, Scott JW and 6 more

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Koentgen F, Lynch GS, Watt MJ, van Denderen BJ, Campbell DJ, Kemp BE

The Journal of biological chemistry20 Sept 2010Cited by 143 (Europe PMC)

PMID20855892 (opens in a new tab)PMCIDPMC2988326 (opens in a new tab)DOI10.1074/jbc.m110.102434 (opens in a new tab)PepBankPUB-20855892
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Summary

AMP-activated protein kinase (AMPK) β subunits (β1 and β2) provide scaffolds for binding α and γ subunits and contain a carbohydrate-binding module important for regulating enzyme activity. We generated C57Bl/6 mice with germline deletion of AMPK β2 (β2 KO) and examined AMPK expression and activity, exercise capacity, metabolic control during muscle contractions, aminoimidazole carboxamide ribonucleotide (AICAR) sensitivity, and susceptibility to obesity-induced insulin resistance. We find that β2 KO mice are viable and breed normally. β2 KO mice had a reduction in skeletal muscle AMPK α1 and α2 expression despite up-regulation of the β1 isoform. Heart AMPK α2 expression was also reduced but this did not affect resting AMPK α1 or α2 activities. AMPK α1 and α2 activities were not changed in liver, fat, or hypothalamus. AICAR-stimulated glucose uptake but not fatty acid oxidation was impaired in β2 KO mice. During treadmill running β2 KO mice had reduced maximal and endurance exercise capacity, which was associated with lower muscle and heart AMPK activity and reduced levels of muscle and liver glycogen. Reductions in exercise capacity of β2 KO mice were not due to lower muscle mitochondrial content or defects in contraction-stimulated glucose uptake or fatty acid oxidation. When challenged with a high-fat diet β2 KO mice gained more weight and were more susceptible to the development of hyperinsulinemia and glucose intolerance. In summary these data show that deletion of AMPK β2 reduces AMPK activity in skeletal muscle resulting in impaired exercise capacity and the worsening of diet-induced obesity and glucose intolerance.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

No result from this study comes from a test of the peptide.

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. 01AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism

    In mice, AMPK β2 deletion impaired AICAR-stimulated glucose uptake.

    In plain wordsIn mice, AMPK β2 deletion reduced glucose uptake stimulated by AICAR compared with controls.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseAICAR-stimulated glucose uptake
    Study

    mousen: not reported in source

    AMPK β2 knockout mice
    Comparator
    wild-type mice
    Outcome group
    Glycemic control · Metabolic and weight

    Source sentences

    Summary
    AICAR-stimulated glucose uptake but not fatty acid oxidation was impaired in β2 KO mice.
    1 context sentence
    Summary · context
    We generated C57Bl/6 mice with germline deletion of AMPK β2 (β2 KO) and examined AMPK expression and activity, exercise capacity, metabolic control during muscle contractions, aminoimidazole carboxamide ribonucleotide (AICAR) sensitivity, and susceptibility to obesity-induced insulin resistance.

    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. 02AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism

    In mice, AMPK β2 deletion did not impair AICAR-stimulated fatty acid oxidation.

    In plain wordsIn mice, AMPK β2 deletion did not impair fat oxidation stimulated by AICAR compared with controls.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeAICAR-stimulated fatty acid oxidation
    Study

    mousen: not reported in source

    AMPK β2 knockout mice
    Comparator
    wild-type mice
    Outcome group
    Lipids · Metabolic and weight

    Source sentences

    Summary
    AICAR-stimulated glucose uptake but not fatty acid oxidation was impaired in β2 KO mice.
    1 context sentence
    Summary · context
    We generated C57Bl/6 mice with germline deletion of AMPK β2 (β2 KO) and examined AMPK expression and activity, exercise capacity, metabolic control during muscle contractions, aminoimidazole carboxamide ribonucleotide (AICAR) sensitivity, and susceptibility to obesity-induced insulin resistance.

    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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