EXERCISE, UNLIKE INSULIN, PROMOTES GLUCOSE-TRANSPORTER TRANSLOCATION IN OBESE ZUCKER RAT MUSCLE

Insulin or exercise stimulates skeletal muscle glucose transport, most likely by increasing both the number and activity of glucose transpor ters in the plasma membrane. Skeletal muscle glucose transport of gene tically obese Zucker rats (fa/fa) displays a severe insulin resistance that results, at least in part, from a failure of net transporter tra nslocation to the cell membrane (King, P., E. D. Horton, M. Hirshman, and E. S. Horton. J. Clin. Invest. 90: 1568-1575, 1992). The purpose o f the present study was to determine if the obese rat muscle was also resistant to the action of acute exercise to increase glucose transpor t and, if so, to determine if the defect involved transporter transloc ation as seen in the resistance to insulin. The muscle glucose transpo rt system was investigated in plasma membranes isolated from postprand ial, sedentary or acutely exercised, lean and obese Zucker rats. Measu rements of D- and L-glucose uptake by membrane vesicles under equilibr ium exchange conditions indicated that an acute bout of exercise resul ted in a threefold increase in the maximum velocity (V(max)) for lean animals (5.7 vs. 17.6 nmol . mg protein-1 . min-1) and a 4.5-fold incr ease in the V(max) for obese rats (4.1 vs. 18.6 nmol . mg protein-1 . min-1). For both lean and obese animals, this increase in transport wa s associated with an increase in transporter number measured by cytoch alasin B binding (1.6- and 2.2-fold, respectively) and with an increas e in the average carrier turnover number (1.9- and 2.0-fold, respectiv ely). The results indicate that, unlike a maximal insulin stimulus, ac ute exercise of the obese Zucker rat promotes both transporter translo cation and transporter activation in skeletal muscle.