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Hypothalamic and peripheral mechanisms involved in metabolic alterations induced by REM sleep deprivation or REM sleep restriction

Grant number: 12/23488-6
Support Opportunities:Regular Research Grants
Duration: April 01, 2013 - March 31, 2015
Field of knowledge:Health Sciences - Medicine - Medical Clinics
Principal Investigator:Deborah Suchecki
Grantee:Deborah Suchecki
Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil


Sleep and feeding behavior are controlled bt the hypothalamus and regulated by numerous hormonal and molecular signals and environmental information. REM sleep deprivation (REMSD) in rats induces hormonal and metabolic changes leading to increased energy intake and loss of body weight. This increased catabolism appears to be mediated by persistent activation of the hypothalamic-pituitary-adrenal (HPA) axis. In addition, prolonged forced waking increases the activity of orexigenic hypothalamic mediators, such as orexin and neurpeptide Y. Little, however, is known about the time-course of changes involving the stress axis and the orexigenic mediators. Therefore, the first goal of the present proposal is to assess the time-course of plasma ACTH, corticosterone, glucose, insulin and leptin, together with the immunoreactivity of corticotropin releasing hormone in the paraventricular nucleus of the hypothalamus and of orexin in the lateral hypothalamic area. Moreover, epidemiological studies have attributed the increased incidence of metabolic syndrome (augmented body weight, insulin resistance syndrome, increased visceral fat depot) to a voluntary sleep curtailment, which results in less than ideal sleep time. Although the peripheral mechanisms that explain the relationship between sleep curtailment and metabolic syndrome in humans is relatively well-known, very little or nothing is known about the central regulation, which makes animal models essencial for this purpose. In rats, however, 21 days of sleep restriction (SR) also leads to loss of body weight, indicating a lack of good "bona fide" models. Our hypothesis to explain this failure is based on the type of diet that is offered to the animals during the SR period. Rats eat standardized chow, whereas studies show that humans subjected to sleep curtailment prefer hypercaloric foods. Thus, the objetive of Experiment 2 is to evaluate whether SR associated with hypercaloric foods induces metabolic syndrome in rats and which the hormonal and peripheral and central signals involved in this process. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
VENANCIO, DANIEL PAULINO; SUCHECKI, DEBORAH. Prolonged REM sleep restriction induces metabolic syndrome-related changes: Mediation by pro-inflammatory cytokines. BRAIN BEHAVIOR AND IMMUNITY, v. 47, n. SI, p. 109-117, . (12/23488-6)
MORAES, DANILO ALVES; VENANCIO, DANIEL PAULINO; SUCHECKI, DEBORAH. Sleep deprivation alters energy homeostasis through non-compensatory alterations in hypothalamic insulin receptors in Wistar rats. Hormones and Behavior, v. 66, n. 5, p. 705-712, . (12/23488-6, 10/14311-0)
ROSSI, VANESSA CONTATTO; TIBA, PAULA AYAKO; MONREIRA, KARIN DI MONTEIRO; FERREIRA, TATIANA LIMA; MENEZES OLIVEIRA, MARIA GABRIELA; SUCHECKI, DEBORAH. Effects of sleep deprivation on different phases of memory in the rat: dissociation between contextual and tone fear conditioning tasks. FRONTIERS IN BEHAVIORAL NEUROSCIENCE, v. 8, . (12/23488-6)

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