Evidence that nitric oxide increases glucose transport in skeletal muscle. Balon, Thomas W., and Jerry L. Nadler. Department of Diabetes, Endocrinology and Metabolism, City of Hope National Medical Center, Duarte, CA 91010, phone: 818-359-8111 extension 2587, FAX:818-301-8489, E-MAIL: TBALON@smtplink.coh.org
APStracts 3:0459A, 1996.
Nitric oxide synthase (NOS) is expressed in skeletal muscle. However, the role of NO in glucose transport in this tissue remains unclear. To determine the role of nitric oxide in modulating glucose transport, 2-deoxyglucose (2-DG) transport was measured in rat extensor digitorum longus (EDL) muscles that were exposed to either a maximally stimulating concentration of insulin or an electrical stimulation protocol, in the presence of NG-monomethyl-L-arginine (L -NMMA), a NOS inhibitor. In addition, EDL preparations were exposed to sodium nitroprusside (SNP), a NO donor, in the presence of submaximal and maximally stimulating concentrations of insulin. NOS inhibition reduced both basal and exercise-enhanced 2-DG transport but had no effect on insulin stimulated 2-DG transport. Furthermore SNP increased 2-deoxyglucose transport in a dose-responsive manner. The effects of SNP and insulin on 2-DG transport were additive when insulin was present in physiological but not pharmacological concentrations. Chronic treadmill training increased protein expression of both Type I and Type III NOS in soleus muscle homogenates. Our results suggest that NO may be a potential mediator of exercise-induced glucose transport. 

Received 7 August 1996; accepted in final form 8 October 1996.
APS Manuscript Number A757-6.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996