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.

Vasopressin and nitric oxide synthesis after three days of water or food deprivation.

Nitric oxide has been suggested to be involved in the regulation of fluid and nutrient homeostasis. In the present investigation, vasopressin and nitric oxide metabolite (nitrite and nitrate) levels were determined in plasma of male Wistar rats submitted to water or food deprivation for three days. Hematocrit and plasma sodium showed marked increase in dehydrated and starved rats. Potassium levels and plasma volume decreased in both treated groups. Plasma osmolality and vasopressin levels were significantly elevated in water deprived (362.8 +/- 7.1 mOsm/kg H2O, 17.3 +/- 2.7 pg/ml, respectively, p < 0.001) rats, but not in food deprived (339.9 +/- 5.0, 1.34 +/- 0.28) rats, compared to the controls (326.1 +/- 4.1, 1.47 +/- 0.32). The alterations observed in plasma vasopressin levels were related to plasma osmolality rather than plasma volume. Plasma levels of nitrite and nitrate were markedly increased in both water and food deprived rats (respectively, 2.19 +/- 0.29 mg/l and 2.22 +/- 0.17 mg/l versus 1.33 +/- 0.19 mg/l, both p < 0.01). There was a significant negative correlation between plasma nitrite and nitrate concentration and plasma volume. These results suggest that both dehydration and starvation increase plasma nitric oxide, probably by activation of nitric oxide synthases. The release of nitric oxide may participate in the regulation of the alteration in blood flow, fluid and nutrient metabolism caused by water deprivation or starvation.

Protective effect of resveratrol on ethanol-induced lipid peroxidation in rats.

AIM: Chronic ethanol treatment induces an increase in oxidative stress. As polyphenolic compounds are potent antioxidants, we aimed to examine whether dietary supplementation of resveratrol may attenuate lipid peroxidation, the major end-point of oxidative damage resulting from chronic ethanol administration. METHOD: Three groups of male Wistar rats were used. The first group served as control and received a daily intraperitoneal injection of 0.9% saline. The second group of rats was daily injected with 35% ethanol at 3 g/kg body weight. The third group was given the same dose of ethanol and supplemented with resveratrol (5 g/kg) in the standard diet. Malondialdehyde (MDA), an indicator of oxidative stress, was measured in the liver, heart, brain, and testis. RESULTS: At the end of a 6 weeks treatment period, MDA levels were significantly increased by 51.5, 53.7, 72.7, and 40.5% in the liver, heart, brain, and testis, respectively. However, when ethanol treated rats were given resveratrol the increase in MDA levels was significantly reduced in all organs to nearly those of control rats. CONCLUSION: Resveratrol is able to inhibit the ethanol-induced lipid peroxidation and have protective effect against oxidative injury.