期刊
CELL METABOLISM
卷 11, 期 1, 页码 58-69出版社
CELL PRESS
DOI: 10.1016/j.cmet.2009.11.009
关键词
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资金
- Gerstner Family Career Development Award
- Mayo Graduate School Fellowship
- American Society for Clinical Pharmacology and Therapeutics Young Investigator Award
- NIH [T32GM008685, RO1HL64822, AR052777]
- Marriott Heart Diseases Research Program
- Marriott Foundation
- Medical Research Initiative Roy J Carver Charitable Trust
- Fraternal Order of Eagles, Iowa Aerie
Metabolic processes that regulate muscle energy use are major determinants of bodily energy balance. Here, we find that sarcolemmal ATP-sensitive K+ (K-ATP) channels, which couple membrane excitability with cellular metabolic pathways, set muscle energy expenditure under physiological stimuli. Disruption of K-ATP channel function provoked, under conditions of unaltered locomotor activity and blood substrate availability, an extra energy cost of cardiac and skeletal muscle performance. Inefficient fuel metabolism in K-ATP channel-deficient striated muscles reduced glycogen and fat body depots, promoting a lean phenotype. The propensity to lesser body weight imposed by K-ATP channel deficit persisted under a high-fat diet, yet obesity restriction was achieved at the cost of compromised physical endurance. Thus, sarcolemmal K-ATP channels govern muscle energy economy, and their downregulation in a tissue-specific manner could present an antiobesity strategy by rendering muscle increasingly thermogenic at rest and less fuel efficient during exercise.
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