ArticleMolecular metabolism2020
Inducible deletion of skeletal muscle AMPKα reveals that AMPK is required for nucleotide balance but dispensable for muscle glucose uptake and fat oxidation during exercise.
Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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30 citing papers in PubMed, 49 citations in OpenAlex.
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- Ampk alpha2 T172 activation dictates exercise performance and energy transduction in skeletal muscle.Science advances · 2026Article
- AMPK/mTOR balance during exercise: implications for insulin resistance in aging muscle.Molecular and cellular biochemistry · 2025Review
- Diminished Motivation for Voluntary Exercise and Metabolic Dysfunction in Psychiatric Disorders: A Behavioral Perspective on Autism Spectrum Disorder and Depression.International neurourology journal · 2025Article
- Cellular Feimin enhances exercise performance by suppressing muscle thermogenesis.Nature metabolism · 2025Article
- Importance of selected genetic determinants on endurance performance and physical strength: a narrative review.Frontiers in physiology · 2025Review
- The metabolic sensor AMPK: Twelve enzymes in one.Molecular metabolism · 2024Review
- Exercise and nutrition benefit skeletal muscle: From influence factor and intervention strategy to molecular mechanism.Sports medicine and health science · 2024Review
- Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry.Journal of visualized experiments : JoVE · 2024Article
- AMPK as a mediator of tissue preservation: time for a shift in dogma?Nature reviews. Endocrinology · 2024Review
- The influence of exercise intensity on comorbid anxious behavior in psychiatric conditions.The journal of physiological sciences : JPS · 2024Article
- AMPK and Beyond: The Signaling Network Controlling RabGAPs and Contraction-Mediated Glucose Uptake in Skeletal Muscle.International journal of molecular sciences · 2024Review
- Skeletal muscle-specific inducible AMPKα1/α2 knockout mice develop muscle weakness, glycogen depletion, and fibrosis that persists during disuse atrophy.American journal of physiology. Endocrinology and metabolism · 2024Article
- Molecular control of endurance training adaptation in male mouse skeletal muscle.Nature metabolism · 2023Article
- The molecular athlete: exercise physiology from mechanisms to medals.Physiological reviews · 2023Review
- Transcriptomic and Metabolomic Profile Analysis of Muscles Reveals Pathways and Biomarkers Involved in Flavor Differences between Caged and Cage-Free Chickens.Foods (Basel, Switzerland) · 2022Article
- Review
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- Illumination of the Endogenous Insulin-Regulated TBC1D4 Interactome in Human Skeletal Muscle.Diabetes · 2022Article
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Authors and funding
22 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveEvidence for AMP-activated protein kinase (AMPK)-mediated regulation of skeletal muscle metabolism during exercise is mainly based on transgenic mouse models with chronic (lifelong) disruption of AMPK function. Findings based on such models are potentially biased by secondary effects related to a chronic lack of AMPK function. To study the direct effect(s) of AMPK on muscle metabolism during exercise, we generated a new mouse model with inducible muscle-specific deletion of AMPKα catalytic subunits in adult mice.
methodsTamoxifen-inducible and muscle-specific AMPKα1/α2 double KO mice (AMPKα imdKO) were generated by using the Cre/loxP system, with the Cre under the control of the human skeletal muscle actin (HSA) promoter.
resultsDuring treadmill running at the same relative exercise intensity, AMPKα imdKO mice showed greater depletion of muscle ATP, which was associated with accumulation of the deamination product IMP. Muscle-specific deletion of AMPKα in adult mice promptly reduced maximal running speed and muscle glycogen content and was associated with reduced expression of UGP2, a key component of the glycogen synthesis pathway. Muscle mitochondrial respiration, whole-body substrate utilization, and muscle glucose uptake and fatty acid (FA) oxidation during muscle contractile activity remained unaffected by muscle-specific deletion of AMPKα subunits in adult mice.
conclusionsInducible deletion of AMPKα subunits in adult mice reveals that AMPK is required for maintaining muscle ATP levels and nucleotide balance during exercise but is dispensable for regulating muscle glucose uptake, FA oxidation, and substrate utilization during exercise.
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