| Literature DB >> 15811316 |
Nicolas Musi1, Michael F Hirshman, Michael Arad, Yanqiu Xing, Nobuharu Fujii, Jason Pomerleau, Ferhaan Ahmad, Charles I Berul, Jon G Seidman, Rong Tian, Laurie J Goodyear.
Abstract
AMP-activated protein kinase (AMPK) plays a critical role in maintaining energy homeostasis and cardiac function during ischemia in the heart. However, the functional role of AMPK in the heart during exercise is unknown. We examined whether acute exercise increases AMPK activity in mouse hearts and determined the significance of these increases by studying transgenic (TG) mice expressing a cardiac-specific dominant-negative (inactivating) AMPKalpha2 subunit. Exercise increased cardiac AMPKalpha2 activity in the wild type mice but not in TG. We found that inactivation of AMPK did not result in abnormal ATP and glycogen consumption during exercise, cardiac function assessed by heart rhythm telemetry and stress echocardiography, or in maximal exercise capacity.Entities:
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Year: 2005 PMID: 15811316 DOI: 10.1016/j.febslet.2005.02.052
Source DB: PubMed Journal: FEBS Lett ISSN: 0014-5793 Impact factor: 4.124