Orexin activation precedes increased NPY expression, hyperphagia, and metabolic changes in response to sleep deprivation

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dc.contributor.author Forcina Martins, Paulo Jose [UNIFESP]
dc.contributor.author Marques, Marina Soares [UNIFESP]
dc.contributor.author Tufik, Sergio [UNIFESP]
dc.contributor.author D'Almeida, Vania [UNIFESP]
dc.date.accessioned 2016-01-24T13:59:22Z
dc.date.available 2016-01-24T13:59:22Z
dc.date.issued 2010-03-01
dc.identifier http://dx.doi.org/10.1152/ajpendo.00660.2009
dc.identifier.citation American Journal of Physiology-endocrinology and Metabolism. Bethesda: Amer Physiological Soc, v. 298, n. 3, p. E726-E734, 2010.
dc.identifier.issn 0193-1849
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/32299
dc.description.abstract Martins PJ, Marques MS, Tufik S, D'Almeida V. Orexin activation precedes increased NPY expression, hyperphagia, and metabolic changes in response to sleep deprivation. Am J Physiol Endocrinol Metab 298: E726-E734, 2010. First published January 5, 2010; doi:10.1152/ajpendo.00660.2009.-Several pieces of evidence support that sleep duration plays a role in body weight control. Nevertheless, it has been assumed that, after the identification of orexins (hypocretins), the molecular basis of the interaction between sleep and energy homeostasis has been provided. However, no study has verified the relationship between neuropeptide Y (NPY) and orexin changes during hyperphagia induced by sleep deprivation. in the current study we aimed to establish the time course of changes in metabolite, endocrine, and hypothalamic neuropeptide expression of Wistar rats sleep deprived by the platform method for a distinct period (from 24 to 96 h) or sleep restricted for 21 days (SR-21d). Despite changes in the stress hormones, we found no changes in food intake and body weight in the SR-21d group. However, sleep-deprived rats had a 25-35% increase in their food intake from 72 h accompanied by slight weight loss. Such changes were associated with increased hypothalamus mRNA levels of prepro-orexin (PPO) at 24 h followed by NPY at 48 h of sleep deprivation. Conversely, sleep recovery reduced the expression of both PPO and NPY, which rapidly brought the animals to a hypophagic condition. Our data also support that sleep deprivation rapidly increases energy expenditure and therefore leads to a negative energy balance and a reduction in liver glycogen and serum triacylglycerol levels despite the hyperphagia. Interestingly, such changes were associated with increased serum levels of glucagon, corticosterone, and norepinephrine, but no effects on leptin, insulin, or ghrelin were observed. in conclusion, orexin activation accounts for the myriad changes induced by sleep deprivation, especially the hyperphagia induced under stress and a negative energy balance. en
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent E726-E734
dc.language.iso eng
dc.publisher Amer Physiological Soc
dc.relation.ispartof American Journal of Physiology-endocrinology and Metabolism
dc.rights Acesso aberto
dc.subject neuropeptide Y en
dc.subject leptin en
dc.subject glucagon en
dc.subject insulin en
dc.subject liver glycogen en
dc.subject triacylglycerol en
dc.title Orexin activation precedes increased NPY expression, hyperphagia, and metabolic changes in response to sleep deprivation en
dc.type Artigo
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Universidade Federal de São Paulo, Dept Psychobiol, BR-04024002 São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Biosci, BR-04024002 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Psychobiol, BR-04024002 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Biosci, BR-04024002 São Paulo, Brazil
dc.description.sponsorshipID FAPESP: 98/14303-3
dc.description.sponsorshipID CNPq: 501248/2005-6
dc.identifier.doi 10.1152/ajpendo.00660.2009
dc.description.source Web of Science
dc.identifier.wos WOS:000274705200036



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