Numerous studies indicate that sleep deprivation alters energy expenditure. However, this conclusion is drawn from indirect measurements. In the present study, we investigated alterations of energy expenditure, body composition, blood glucose levels, plasma insulin, adrenocorticotropic hormone (ACTH) and corticosterone levels immediately after 4 days of sleep deprivation or after 4 days of sleep recovery. Rats were sleep deprived or maintained in a control environment (groups sleep-deprived/deprivation and control/deprivation). One half of these animals were sacrificed at the end of the deprivation period and the other half was transported to metabolic cages, where they were allowed to sleep freely (groups sleep-deprived/recovery and control/recovery). At the end of the sleep recovery period, these rats were sacrificed. After sleep deprivation, sleep-deprived rats exhibited loss of body weight, augmented energy expenditure and reduced metabolic efficiency compared to control rats. These alterations were normalised during the sleep recovery period. The body composition of sleep-deprived rats was altered insofar as there was a loss of fat content and gain of protein content in the carcass compared to control rats. However, these alterations were not reversed by sleep recovery. Finally, plasma levels of insulin were reduced during the sleep deprivation period in both control and sleep deprived groups compared to the recovery period. After the deprivation period, plasma ACTH and corticosterone levels were increased in sleep-deprived rats compared to control rats, and although ACTH levels were similar between the groups after the sleep recovery period, corticosterone levels remained elevated in sleep-deprived rats after this period. By means of direct measurements of metabolism, our results showed that sleep deprivation produces increased energy expenditure and loss of fat content. Most of the alterations were reversed by sleep recovery, except for corticosterone levels and body composition.

OBJECTIVE-Kinins mediate pathophysiological processes related to hypertension, pain, and inflammation through the activation of two G-protein-coupled receptors, named B 1 and B 2 . Although these peptides have been related to glucose homeostasis, their effects on energy balance are still unknown.RESEARCH DESIGN AND METHODS-Using genetic and pharmacological strategies to abrogate the kinin B 1 receptor in different animal models of obesity, here we present evidence of a novel role for kinins in the regulation of satiety and adiposity. RESULTS-Kinin B 1 receptor deficiency in mice (B 1Ϫ/Ϫ ) resulted in less fat content, hypoleptinemia, increased leptin sensitivity, and robust protection against high-fat diet-induced weight gain. Under high-fat diet, B 1 Ϫ/Ϫ also exhibited reduced food intake, improved lipid oxidation, and increased energy expenditure. Surprisingly, B 1 receptor deficiency was not able to decrease food intake and adiposity in obese mice lacking leptin (ob/ob-B 1 Ϫ/Ϫ ). However, ob/ob-B 1 Ϫ/Ϫ mice were more responsive to the effects of exogenous leptin on body weight and food intake, suggesting that B 1 receptors may be dependent on leptin to display their metabolic roles. Finally, inhibition of weight gain and food intake by B 1 receptor ablation was pharmacologically confirmed by long-term administration of the kinin B 1 receptor antagonist SSR240612 to mice under high-fat diet.CONCLUSIONS-Our data suggest that kinin B 1 receptors participate in the regulation of the energy balance via a mechanism that could involve the modulation of leptin sensitivity.

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