Melatonin acts through MT1/MT2 receptors to activate hypothalamic Akt and suppress hepatic gluconeogenesis in rats

dc.creatorFaria, JA
dc.creatorKinote, A
dc.creatorIgnacio-Souza, LM
dc.creatorde Araujo, TM
dc.creatorRazolli, DS
dc.creatorDoneda, DL
dc.creatorPaschoal, LB
dc.creatorLellis-Santos, C
dc.creatorBertolini, GL
dc.creatorVelloso, LA
dc.creatorBordin, S
dc.creatorAnhe, GF
dc.date2013
dc.dateJUL
dc.date2014-07-30T13:40:59Z
dc.date2015-11-26T17:21:04Z
dc.date2014-07-30T13:40:59Z
dc.date2015-11-26T17:21:04Z
dc.date.accessioned2018-03-29T00:08:37Z
dc.date.available2018-03-29T00:08:37Z
dc.identifierAmerican Journal Of Physiology-endocrinology And Metabolism. Amer Physiological Soc, v. 305, n. 2, n. E230, n. E242, 2013.
dc.identifier0193-1849
dc.identifierWOS:000321902000007
dc.identifier10.1152/ajpendo.00094.2013
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/53572
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/53572
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1283284
dc.descriptionMelatonin can contribute to glucose homeostasis either by decreasing gluconeogenesis or by counteracting insulin resistance in distinct models of obesity. However, the precise mechanism through which melatonin controls glucose homeostasis is not completely understood. Male Wistar rats were administered an intracerebroventricular (icv) injection of melatonin and one of following: an icv injection of a phosphatidylinositol 3-kinase (PI3K) inhibitor, an icv injection of a melatonin receptor (MT) antagonist, or an intraperitoneal (ip) injection of a muscarinic receptor antagonist. Anesthetized rats were subjected to pyruvate tolerance test to estimate in vivo glucose clearance after pyruvate load and in situ liver perfusion to assess hepatic gluconeogenesis. The hypothalamus was removed to determine Akt phosphorylation. Melatonin injections in the central nervous system suppressed hepatic gluconeogenesis and increased hypothalamic Akt phosphorylation. These effects of melatonin were suppressed either by icv injections of PI3K inhibitors and MT antagonists and by ip injection of a muscarinic receptor antagonist. We conclude that melatonin activates hypothalamus-liver communication that may contribute to circadian adjustments of gluconeogenesis. These data further suggest a physiopathological relationship between the circadian disruptions in metabolism and reduced levels of melatonin found in type 2 diabetes patients.
dc.descriptiono TEXTO COMPLETO DESTE ARTIGO, ESTARÁ DISPONÍVEL À PARTIR DE AGOSTO DE 2015.
dc.description305
dc.description2
dc.descriptionE230
dc.descriptionE242
dc.descriptionResearch Foundation of the State of Sao Paulo
dc.descriptionNational Council of Research
dc.languageen
dc.publisherAmer Physiological Soc
dc.publisherBethesda
dc.publisherEUA
dc.relationAmerican Journal Of Physiology-endocrinology And Metabolism
dc.relationAm. J. Physiol.-Endocrinol. Metab.
dc.rightsembargo
dc.sourceWeb of Science
dc.subjectmelatonin
dc.subjectgluconeogenesis
dc.subjectmelatonin receptors
dc.subjectliver
dc.subjectCerebrospinal-fluid
dc.subjectGlucose-production
dc.subjectInsulin-resistance
dc.subjectFood-intake
dc.subjectIn-vivo
dc.subjectHyperglycemia
dc.subjectAdipocytes
dc.subjectExpression
dc.subjectPathway
dc.subjectLeptin
dc.titleMelatonin acts through MT1/MT2 receptors to activate hypothalamic Akt and suppress hepatic gluconeogenesis in rats
dc.typeArtículos de revistas


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