Produção Nacional
Revisado por pares
Melatonin acts through MT1/MT2 receptors to activate hypothalamic Akt and suppress hepatic gluconeogenesis in rats
2013; American Physiological Society; Volume: 305; Issue: 2 Linguagem: Inglês
10.1152/ajpendo.00094.2013
ISSN1522-1555
AutoresJuliana A. Faria, Andrezza Pinheiro Bezerra de Menezes Kinote, Letícia Martins Ignácio-Souza, Thiago M. de Araújo, Daniela S. Razolli, Diego Luiz Doneda, Lívia B. Paschoal, Camilo Lellis‐Santos, Gisele Lopes Bertolini, Lı́cio A. Velloso, Silvana Bordin, Gabriel Forato Anhê,
Tópico(s)Regulation of Appetite and Obesity
ResumoMelatonin 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.
Referência(s)