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Study · Animal study (in vivo) · 2015

2 results

Activation of AMPKα2 Is Not Required for Mitochondrial FAT/CD36 Accumulation during Exercise.

Monaco C, Whitfield J, Jain SS, Spriet LL, Bonen A, Holloway GP

PloS one12 May 2015Cited by 15 (Europe PMC)

PMID25965390 (opens in a new tab)PMCIDPMC4429092 (opens in a new tab)DOI10.1371/journal.pone.0126122 (opens in a new tab)PepBankPUB-25965390
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Summary

Exercise has been shown to induce the translocation of fatty acid translocase (FAT/CD36), a fatty acid transport protein, to both plasma and mitochondrial membranes. While previous studies have examined signals involved in the induction of FAT/CD36 translocation to sarcolemmal membranes, to date the signaling events responsible for FAT/CD36 accumulation on mitochondrial membranes have not been investigated. In the current study muscle contraction rapidly increased FAT/CD36 on plasma membranes (7.5 minutes), while in contrast, FAT/CD36 only increased on mitochondrial membranes after 22.5 minutes of muscle contraction, a response that was exercise-intensity dependent. Considering that previous research has shown that AMP activated protein kinase (AMPK) α2 is not required for FAT/CD36 translocation to the plasma membrane, we investigated whether AMPK α2 signaling is necessary for mitochondrial FAT/CD36 accumulation. Administration of 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) induced AMPK phosphorylation, and resulted in FAT/CD36 accumulation on SS mitochondria, suggesting AMPK signaling may mediate this response. However, SS mitochondrial FAT/CD36 increased following acute treadmill running in both wild-type (WT) and AMPKα 2 kinase dead (KD) mice. These data suggest that AMPK signaling is not required for SS mitochondrial FAT/CD36 accumulation. The current data also implicates alternative signaling pathways that are exercise-intensity dependent, as IMF mitochondrial FAT/CD36 content only occurred at a higher power output. Taken altogether the current data suggests that activation of AMPK signaling is sufficient but not required for exercise-induced accumulation in mitochondrial FAT/CD36.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In the muscle study, AICAR induced AMPK phosphorylation.

    In plain wordsIn animals, AICAR increased AMPK phosphorylation in the muscle study.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseAMPK phosphorylation
    Study

    n: not reported in source

    Skeletal muscle
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) induced AMPK phosphorylation, and resulted in FAT/CD36 accumulation on SS mitochondria, suggesting AMPK signaling may mediate this response.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In the muscle study, AICAR caused FAT/CD36 accumulation on subsarcolemmal mitochondria.

    In plain wordsIn animals, AICAR increased FAT/CD36 on mitochondria near the muscle-cell membrane.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseSubsarcolemmal mitochondrial FAT/CD36
    Study

    n: not reported in source

    Skeletal muscle
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) induced AMPK phosphorylation, and resulted in FAT/CD36 accumulation on SS mitochondria, suggesting AMPK signaling may mediate this response.

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Version history

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  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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