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首页> 外文期刊>American Journal of Physiology >Melatonin acts through MT1/MT2 receptors to activate hypothalamic Akt and suppress hepatic gluco-neogenesis in rats.
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Melatonin acts through MT1/MT2 receptors to activate hypothalamic Akt and suppress hepatic gluco-neogenesis in rats.

机译：褪黑素通过MT1 / MT2受体起作用，激活下丘脑Akt并抑制大鼠肝糖异生。

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Melatonin 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.
机译：褪黑激素可以通过减少糖异生或通过在不同的肥胖模型中抵消胰岛素抵抗来促进葡萄糖稳态。但是，尚不完全了解褪黑激素控制葡萄糖稳态的确切机制。对雄性Wistar大鼠进行脑室内（icv）褪黑激素注射和以下操作之一：icv注射磷脂酰肌醇3-激酶（PI3K）抑制剂，icv注射褪黑激素受体（MT）拮抗剂或腹膜内（ip）毒蕈碱受体拮抗剂的注射。麻醉的大鼠接受丙酮酸耐受性试验，以评估丙酮酸负荷后的体内葡萄糖清除率，并进行原位肝灌注以评估肝糖异生。去除下丘脑以确定Akt磷酸化。在中枢神经系统中注射褪黑素可抑制肝糖异生，并增加下丘脑Akt磷酸化。静脉注射PI3K抑制剂和MT拮抗剂以及腹腔注射毒蕈碱受体拮抗剂可抑制褪黑激素的这些作用。我们得出的结论是，褪黑激素激活下丘脑-肝脏的沟通，这可能有助于糖原异生的昼夜调节。这些数据进一步暗示了在2型糖尿病患者中发现的生物节律紊乱与褪黑激素水平降低之间的生理病理关系。

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