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Am J Physiol Endocrinol Metab 290: E925-E932, 2006. First published December 13, 2005; doi:10.1152/ajpendo.00429.2005
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LKB1-AMPK signaling in muscle from obese insulin-resistant Zucker rats and effects of training

Apiradee Sriwijitkamol,1,2 John L. Ivy,3 Christine Christ-Roberts,1 Ralph A. DeFronzo,1,2 Lawrence J. Mandarino,1 and Nicolas Musi1,2

1Diabetes Division, University of Texas Health Science Center at San Antonio; 2Texas Diabetes Institute, San Antonio; and 3Exercise Physiology and Metabolism Laboratory, Department of Kinesiology and Health Education, University of Texas at Austin, Austin, Texas

Submitted 7 September 2005 ; accepted in final form 8 December 2005

AMPK is a key regulator of fat and carbohydrate metabolism. It has been postulated that defects in AMPK signaling could be responsible for some of the metabolic abnormalities of type 2 diabetes. In this study, we examined whether insulin-resistant obese Zucker rats have abnormalities in the AMPK pathway. We compared AMPK and ACC phosphorylation and the protein content of the upstream AMPK kinase LKB1 and the AMPK-regulated transcriptional coactivator PPAR{gamma} coactivator-1 (PGC-1) in gastrocnemius of sedentary obese Zucker rats and sedentary lean Zucker rats. We also examined whether 7 wk of exercise training on a treadmill reversed abnormalities in the AMPK pathway in obese Zucker rats. In the obese rats, AMPK phosphorylation was reduced by 45% compared with lean rats. Protein expression of the AMPK kinase LKB1 was also reduced in the muscle from obese rats by 43%. In obese rats, phosphorylation of ACC and protein expression of PGC-1{alpha}, two AMPK-regulated proteins, tended to be reduced by 50 (P = 0.07) and 35% (P = 0.1), respectively. There were no differences in AMPK{alpha}1, -{alpha}2, -beta1, -beta2, and -{gamma}3 protein content between lean and obese rats. Training caused a 1.5-fold increase in AMPK{alpha}1 protein content in the obese rats, although there was no effect of training on AMPK phosphorylation and the other AMPK isoforms. Furthermore, training also significantly increased LKB1 and PGC-1{alpha} protein content 2.8- and 2.5-fold, respectively, in the obese rats. LKB1 protein strongly correlated with hexokinase II activity (r = 0.75, P = 0.001), citrate synthase activity (r = 0.54, P = 0.02), and PGC-1{alpha} protein content (r = 0.81, P < 0.001). In summary, obese insulin-resistant rodents have abnormalities in the LKB1-AMPK-PGC-1 pathway in muscle, and these abnormalities can be restored by training.

acetyl-CoA carboxylase; peroxisome proliferator-activated receptor-{gamma} coactivator-1{alpha}; exercise



Address for reprint requests and other correspondence: N. Musi, 701 S. Zarzamora, MS 10–5, San Antonio, TX 78207 (e-mail: Nicolas.musi{at}uhs-sa.com)




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