Interaction of exercise training and clenbuterol on glut4 protein in muscle of obese zucker rats. Kuo, Chia-Hua, Zhenping Ding, and John L. Ivy. Exercise Physiology and Metabolism Laboratory, Department of Kinesiology, The University of Texas at Austin, Austin, Texas
APStracts 3:0159E, 1996.
Chronic administration of clenbuterol, a [beta]2-adrenergic agonist, attenuates the exercise training-induced improvement in muscle insulin resistance of the obese Zucker rat. The present study was conducted to determine if clenbuterol also attenuates the increase in muscle GLUT4 protein which occurs with exercise training, and to determine if the action of clenbuterol is related to its ability to down regulate the [beta]-adrenergic receptors. Female, obese Zucker rats were randomly assigned to one of the following four groups: control (CON, n=7), clenbuterol (CL, n=8), exercise training (TR, n=8) and clenbuterol with exercise training (CL+TR, n=8). Rats assigned to the training groups were run on a rodent, motor-driven treadmill for 6-7 wk. Rats receiving clenbuterol were intubated with 0.8 mg/kg body weight 30 min before running each day. Red quadriceps (RQ) and white quadriceps (WQ) GLUT4 protein concentrations of TR rats were significantly greater than CON, and CL+TR rats. The RQ GLUT4 protein concentration of the CL+TR rats was significantly greater than CON, but this difference did not occur in the WQ. GLUT4 protein concentrations were not difference between the CON and CL rats. The patterns of RQ and WQ GLUT4 mRNA were similar to that of their GLUT4 proteins, respectively. Rats receiving daily injections of propranolol (30 mg/kg body wt), a [beta]-adrenergic receptor antagonist, demonstrated no increase in GLUT4 protein in RQ or WQ after 6 wk of exercise training. These results indicate that, 1) clenbuterol can attenuate the increase in muscle GLUT4 protein associated with exercise training, and 2) that this effect is likely mediated by a down regulation of the [beta]-adrenergic receptors.

Received 16 January 1996; accepted in final form 26 June 1996.
APS Manuscript Number E16-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 21 August 1996