EVIDENCE THAT NITRIC-OXIDE INCREASES GLUCOSE-TRANSPORT IN SKELETAL-MUSCLE

Nitric oxide synthase (NOS) is expressed in skeletal muscle. However, the role of nitric oxide (NO) in glucose transport in this tissue rema ins unclear. To determine the role of NO in modulating glucose transpo rt, 2-deoxyglucose (2-DG) transport was measured in rat extensor digit orum longus (EDL) muscles that were exposed to either a maximally stim ulating concentration of insulin or to an electrical stimulation proto col, in the presence of N-G-monomethyl-L-arginine, a NOS inhibitor. In addition, EDL preparations were exposed to sodium nitroprusside (SNP) , an NO donor, in the presence of submaximal and maximally stimulating concentrations of insulin. NOS inhibition reduced both basal and exer cise-enhanced 2-DG transport but had no effect on insulin-stimulated 2 -DG transport. Furthermore, SNP increased 2-DG transport in a dose-res ponsive manner. The effects of SNP and insulin on 2-DG transport were additive when insulin was present in physiological but not in pharmaco logical concentrations. Chronic treadmill training increased protein e xpression 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.