Exercise training reverses insulin resistance in muscle by enhanced recruitment of glut4 to the cell surface. Etgen, Garret J., J[phi]rgen Jensen, Cindy M. Wilson, Desmond G. Hunt, Samuel W. Cushman, and John L. Ivy. Exercise Physiology and Metabolism Laboratory, Department of Kinesiology, University of Texas at Austin, Austin, TX 78712, and the Experimental Diabetes, Metabolism, and Nutrition Section, DB/NIDDK, National Institutes of Health, Bethesda, MD 20892
APStracts 4:0029E, 1997.
The effects of exercise training on cell surface GLUT4 in skeletal muscle of the obese (fa/fa) Zucker rat were investigated using the impermeant glucose transporter photoaffinity reagent 2-N-4-(l-azi -2,2,2-trifluoroethyl)benzoyl-1,3-bis-(D-mannos-4-yloxy)-2-propylamine (ATB-BMPA). In the absence of insulin, 3-O-methyl-D-glucose transport activity was no different in either fast-twitch (epitrochlearis) or slow-twitch (soleus) muscles of trained and sedentary obese rats. Likewise, basal ATB-BMPA-labelled GLUT4 was not altered in these muscles with training. In contrast, the trained group exhibited significantly greater insulin-stimulated (2 mU/ml) glucose transport activity in epitrochlearis muscles than the sedentary group (0.53 +/- 0.03 [mu]mol/g/10 min vs. 0.18 +/- 0.03 [mu]mol/g/10 min for trained and sedentary, respectively) which was paralleled by a significant enhancement of insulin-stimulated cell surface GLUT4 (5.33 +/- 0.20 dpm/mg vs. 1.57 +/- 0.14 dpm/mg for trained and sedentary, respectively). Exercise training, however, did not alter insulin -stimulated glucose transport activity or cell surface GLUT4 in soleus muscles. Finally, exercise training did not alter the ability of muscle contraction to elevate glucose transport activity or cell surface GLUT4 in either epitrochlearis or soleus muscles of the obese rat. These results indicate that training improves insulin-stimulated glucose transport in muscle of the obese Zucker rat by increasing GLUT4 content and altering the normal intracellular distribution of these transporters such that they are now capable of migrating to the cell surface in response to the insulin stimulus. 

Received 7 October 1996; accepted in final form 16 January 1997.
APS Manuscript Number E501-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 19 February 1997