APPS November 2002 Meeting Abstract 1221


Sean L. McGee1, Kirsten F. Howlett1, Rebecca L. Starkie1, David Cameron-Smith1, Bruce E. Kemp2, Mark Hargreaves1, 1 Exercise, Muscle and Metabolism Unit, School of Health Sciences, Deakin University, Burwood, Victoria, 2 St. Vincent's Institute of Medical Research, St. Vincent's Hospital, Fitzroy, Victoria.

Skeletal muscle glucose transport is primarily mediated by the transmembrane glucose transporter GLUT-4. Overexpression of GLUT-4 in skeletal muscle improves whole body insulin action and glucose homeostasis1, 2. Consequently, increasing skeletal muscle GLUT-4 is seen as a potential mechanism to treat and manage type 2 diabetes. Exercise is known to increase both GLUT-4 gene3 and protein4 expression. Recent studies have shown an association between increased GLUT-4 expression and the AMP-activated protein kinase (AMPK)5, 6, the activity of which is increased in response to exercise7. AMPK activation has also been associated with enhanced expression of other metabolic genes, such as mitochondrial enzymes8. It has been hypothesised that AMPK might regulate gene expression through direct interaction with the nucleus. The purpose of this study was to determine if nuclear AMPK α2 content was increased in human skeletal muscle, in response to an exercise bout that we have previously found to increase GLUT-4 gene expression3. Six male subjects (20.62.1 yrs; 72.92.1 kg; 1803 cm, VO2peak = 3.620.18 l.min-1) cycled for 60 min at 721% of VO2peak. Immediately after exercise, nuclear AMPK α2 content was increased 1.90.4 fold (p = 0.024). There was no change in whole cell AMPK α2 content or AMPK α2 mRNA abundance. These results suggest that the nuclear translocation of AMPK might mediate the effects of exercise on skeletal muscle gene and protein expression.

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