APStracts 4:0092E, 1997.

Exercise-stimulated glucose transport in skeletal muscle is nitric oxide dependent. Roberts, Christian K., R. James Barnard, Stephen H. Scheck, and Thomas W. Balon. Department of Physiological Science, University of California, Los Angeles, California, 90024

APStracts 4:0092E, 1997.

It has been suggested that there are separate insulin-stimulated and contraction-stimulated glucose transport pathways in skeletal muscle. This study examined the effects of nitric oxide on glucose transport in rat skeletal muscle using an isolated sarcolemmal membrane preparation and the nitric oxide synthase inhibitor, N(-nitro-L -arginine methyl ester (L-NAME), administered in the drinking water (1 mg/ml). Female Sprague-Dawley rats were divided into five groups: control, acute exercise, acute exercise + L-NAME, insulin-stimulated, and insulin-stimulated + L-NAME. Exercise (45 min of exhaustive treadmill running) increased glucose transport (37(2 to 76(5 pmol.mg -1.15s-1), and this increase was completely inhibited by L-NAME (40(4 pmol.mg-1.15s-1). A maximum dose of insulin increased glucose transport (87(10 pmol.mg-1.15s-1), and adding L-NAME had no effect (87(11 pmol.mg-1.15s-1). In addition, exercise, but not exercise + L -NAME, increased sarcolemma GLUT-4 content. This study confirms that there are separate pathways for contraction- and insulin-stimulated glucose transport. More importantly, while exercise and insulin both significantly increased glucose transport, L-NAME had no effect on insulin-stimulated glucose transport but blocked the exercise -stimulated transport. We conclude that nitric oxide is involved in the signal transduction mechanism to increase glucose transport during exercise.

Received 4 April 1997; accepted in final form 11 April 1997.
APS Manuscript Number E53-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 13 May 1997