Involvement of Nitric Oxide in Corticosterone Release and Glucose Metabolism in Food Deprived Rats

This study was performed to investigate the involvement of nitric oxide (NO) in corticosterone, endpoint product of hypothalamo-pituitary-adrenal (HPA) axis activation, and metabolic responses to 3 days of food deprivation. To investigate this aim, we used a nonspecific inhibitor of nitric oxide synthases, N-nitro-L-arginine methyl ester (L-NAME). In food deprived group we have noted a significant increase in plasma corticosterone concentration accompanied by a significant depletion in hepatic glycogen content with concomitant increase in glycogen phosphorylase (GP) activity by 63.72 %, key enzyme of glycogenolysis and decrease in hexokinase (HK) activity by 25.16 %, leading to significant decrease in glucose concentration. However, L-NAME administration in food deprived rats decreased slightly corticosterone level and GP activity (16.39 %) and increased HK activity (11.26 %) as compared to food deprived group. Considering these results, we can deduce that in food deprivation nitric oxide is involved in the regulation of corticosterone release and in glucose metabolic responses via glycogenolysis activation by the stimulation of GP activity and the inhibition of HK activity. However, more studies are necessary to further clarify the mechanisms by which NO induces these responses.