| Obesity impairs skeletal muscle AMPK signaling during exercise: role of AMPKα2 in the regulation of exercise capacity in vivo. | |
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MedLine Citation:
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PMID: 21079619 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Objective:Skeletal muscle AMP-activated protein kinase (AMPK)α2 activity is impaired in obese, insulin-resistant individuals during exercise. We determined whether this defect contributes to the metabolic dysregulation and reduced exercise capacity observed in the obese state.Design:C57BL/6J wild-type (WT) mice and/or mice expressing a kinase dead AMPKα2 subunit in skeletal muscle (α2-KD) were fed chow or high-fat (HF) diets from 3 to 16 weeks of age. At 15 weeks, mice performed an exercise stress test to determine exercise capacity. In WT mice, muscle glucose uptake and skeletal muscle AMPKα2 activity was assessed in chronically catheterized mice (carotid artery/jugular vein) at 16 weeks. In a separate study, HF-fed WT and α2-KD mice performed 5 weeks of exercise training (from 15 to 20 weeks of age) to test whether AMPKα2 is necessary to restore work tolerance.Results:HF-fed WT mice had reduced exercise tolerance during an exercise stress test, and an attenuation in muscle glucose uptake and AMPKα2 activity during a single bout of exercise (P<0.05 versus chow). In chow-fed α2-KD mice, running speed and time were impaired ∼45 and ∼55%, respectively (P<0.05 versus WT chow); HF feeding further reduced running time ∼25% (P<0.05 versus α2-KD chow). In response to 5 weeks of exercise training, HF-fed WT and α2-KD mice increased maximum running speed ∼35% (P<0.05 versus pre-training) and maintained body weight at pre-training levels, whereas body weight increased in untrained HF WT and α2-KD mice. Exercise training restored running speed to levels seen in healthy, chow-fed mice.Conclusion:HF feeding impairs AMPKα2 activity in skeletal muscle during exercise in vivo. Although this defect directly contributes to reduced exercise capacity, findings in HF-fed α2-KD mice show that AMPKα2-independent mechanisms are also involved. Importantly, α2-KD mice on a HF-fed diet adapt to regular exercise by increasing exercise tolerance, demonstrating that this adaptation is independent of skeletal muscle AMPKα2 activity. |
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Authors:
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R S Lee-Young; J E Ayala; P T Fueger; W H Mayes; L Kang; D H Wasserman |
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Publication Detail:
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Type: Journal Article Date: 2010-11-16 |
Journal Detail:
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Title: International journal of obesity (2005) Volume: 35 ISSN: 1476-5497 ISO Abbreviation: Int J Obes (Lond) Publication Date: 2011 Jul |
Date Detail:
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Created Date: 2011-07-12 Completed Date: 2011-09-14 Revised Date: 2012-04-20 |
Medline Journal Info:
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Nlm Unique ID: 101256108 Medline TA: Int J Obes (Lond) Country: England |
Other Details:
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Languages: eng Pagination: 982-9 Citation Subset: IM |
Affiliation:
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Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA. |
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| MeSH Terms | |
Descriptor/Qualifier:
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AMP-Activated Protein Kinases
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metabolism* Animals Dietary Fats / administration & dosage Exercise Tolerance / physiology Female Male Mice Mice, Inbred C57BL Obesity / metabolism*, physiopathology Physical Conditioning, Animal / physiology* Signal Transduction |
| Grant Support | |
ID/Acronym/Agency:
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R01 DK054902-12/DK/NIDDK NIH HHS; R01 DK054902-13/DK/NIDDK NIH HHS; U24 DK059637-10/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Dietary Fats; EC 2.7.11.1/AMP-Activated Protein Kinases; EC 2.7.11.1/AMPK alpha2 subunit, mouse |
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