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血糖浓度调控中的神经机制。

Neural mechanisms in the control of blood glucose concentration.

作者信息

Niijima A

机构信息

Department of Physiology, Niigata University School of Medicine, Japan.

出版信息

J Nutr. 1989 Jun;119(6):833-40. doi: 10.1093/jn/119.6.833.

Abstract

Recent studies of sensory signals from the visceral areas have enhanced our understanding of mechanisms that control blood glucose levels. The activity of efferent fibers to the pancreas, liver, and adrenal medulla is modulated by both central glucose-responsive neurons and peripheral (gustatory, intestinal and hepatic) glucose sensors. It is well known that induction of hyperglycemia facilitates efferent activity of the pancreatic and hepatic branches of the vagus nerve. This in turn increases insulin secretion from the pancreas and glycogen synthesis in the liver. Hypoglycemia activates efferent activity of the pancreatic, hepatic and adrenal branches of the splanchnic nerve, and this results in increased glucagon secretion from the pancreas, release of glucose from the liver and secretion of catecholamines from the adrenal medulla. Glucose-responsive neurons in the hypothalamus and medulla oblongata may be involved in the modulation of this autonomic efferent activity.

摘要

近期对来自内脏区域感觉信号的研究增进了我们对控制血糖水平机制的理解。支配胰腺、肝脏和肾上腺髓质的传出纤维的活动受到中枢葡萄糖反应性神经元和外周(味觉、肠道和肝脏)葡萄糖传感器的调节。众所周知,高血糖的诱导会促进迷走神经胰腺和肝脏分支的传出活动。这反过来又会增加胰腺的胰岛素分泌和肝脏中的糖原合成。低血糖会激活内脏神经胰腺、肝脏和肾上腺分支的传出活动,这会导致胰腺中胰高血糖素分泌增加、肝脏中葡萄糖释放以及肾上腺髓质中儿茶酚胺分泌增加。下丘脑和延髓中的葡萄糖反应性神经元可能参与了这种自主传出活动的调节。

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