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Department of Diabetes, Endocrinology, and Metabolism, City of Hope National Medical Center, Duarte, California 91010
Received 7 August 1996; accepted in final form 8 October 1996.
Balon, Thomas W., and Jerry L. Nadler. Evidence that
nitric oxide increases glucose transport in skeletal muscle.
J. Appl. Physiol. 82(1): 359-363, 1997.
Nitric oxide synthase (NOS) is expressed in skeletal muscle.
However, the role of nitric oxide (NO) in glucose transport in this
tissue remains unclear. To determine the role of NO 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 to an electrical
stimulation protocol, in the presence of
NG-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 exercise-enhanced 2-DG transport but had no effect on
insulin-stimulated 2-DG transport. Furthermore, SNP increased 2-DG
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 in 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.
insulin; nitric oxide synthase isoforms; treadmill running; sodium nitroprusside; 2-deoxyglucose transport
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