CHRONIC GROWTH-HORMONE TREATMENT IN NORMAL RATS REDUCES POSTPRANDIAL SKELETAL-MUSCLE PLASMA-MEMBRANE GLUT1 CONTENT, BUT NOT GLUCOSE-TRANSPORT OR GLUT4 EXPRESSION AND LOCALIZATION

Whether skeletal muscle glucose transport system is impaired in the ba sal, post-prandial state during chronic growth hormone treatment is un known. The current study was designed to determine whether 4 weeks of human growth hormone (hGH) treatment (3.5 mg/kg per day) would impair glucose transport and/or the number of glucose transporters in plasma membrane vesicles isolated from hindlimb skeletal muscle of Sprague-Da wley rats under basal, post-prandial conditions. hGH treatment was sho wn to have no effect on glucose influx (V-max or K-m) determined under equilibrium exchange conditions in isolated plasma membrane vesicles. Plasma membrane glucose transporter number (R(o)) measured by cytocha lasin B binding was also unchanged by hGH treatment. Consequently, glu cose transporter turnover number (V-max/R(o)), a measure of average gl ucose transporter intrinsic activity, was similar in hGH-treated and c ontrol rats. hGH did not change GLUT4 protein content in whole muscle or in the plasma membrane, and muscle content of GLUT4 mRNA also was u nchanged. In contrast, GLUT1 protein content in the plasma membrane fr action was significantly reduced by hGH treatment, This was associated with a modest, although not significant, decrease in muscle content o f GLUT1 mRNA. In conclusion, high-dose hGH treatment for 4 weeks did n ot alter post-prandial skeletal muscle glucose transport activity, Nei ther the muscle level nor the intracellular localization of GLUT4 was changed by the hormone treatment. On the contrary, the basal post-pran dial level of GLUT1 in the plasma membrane was reduced by hGH. The mRN A data suggest that this reduction might result from a decrease in the synthesis of GLUT1.