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Department of Physiology and Lipid Research Unit, Laval University Hospital Research Center, Saint-Foy, Quebec, Canada G1V 4G2
The purpose of this
study was to investigate whether in vivo nitric oxide synthase (NOS)
inhibition influences insulin-mediated glucose disposal in rat
peripheral tissues. The NOS inhibitor NG-nitro-L-arginine methyl ester
(L-NAME) or saline was infused constantly during a hyperinsulinemic-euglycemic clamp in normal rats.
Glucose utilization rates of insulin-sensitive tissues (individual muscles, heart, and adipose tissues) were simultaneously determined using tracer infusion of
2-deoxy-D-[3H]glucose
(2-[3H]DG). NOS
blockade with L-NAME resulted in
significant (P < 0.05) reduction in
both whole body glucose disposal (
16%,
P < 0.01) and plasma
2-[3H]DG disappearance
rate (30%, P < 0.05) during
hyperinsulinemic-euglycemic clamp.
L-NAME significantly decreased
insulin-stimulated glucose uptake in heart (62%,
P = 0.01), soleus
(42%, P = 0.05), red (53%, P < 0.001) and white
(62%, P < 0.001)
gastrocnemius, tibialis (57%,
P < 0.01), and quadriceps
(33%, P < 0.05) muscles. The NOS inhibitor also decreased insulin action in brown interscapular (47%, P < 0.01),
retroperitoneal (52%, P = 0.07), and gonadal (66%, P = 0.06) adipose tissues. In contrast to in vivo NOS blockade, L-NAME failed to affect basal or
insulin-stimulated
2-[3H]DG transport in
isolated soleus or extensor digitorum longus muscles in vitro. These
results support the hypothesis that the action of insulin to augment
glucose uptake by skeletal muscles and other peripheral
insulin-sensitive tissues in vivo is NO dependent.
endothelial-type nitric oxide synthase; neuronal-type nitric oxide synthase; endothelium; vascular beds; soleus; extensor digitorum longus; nitric oxide
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