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下丘脑和遗传性肥胖啮齿动物高胰岛素血症中传出迷走神经核的起源及作用

The origins and role of efferent vagal nuclei in hyperinsulinemia in hypothalamic and genetically obese rodents.

作者信息

Rohner-Jeanrenaud F, Ionescu E, Jeanrenaud B

出版信息

J Auton Nerv Syst. 1983 Oct;9(1):173-84. doi: 10.1016/0165-1838(83)90139-x.

Abstract

The main brainstem parasympathetic efferent neurons that ultimately reach the pancreas and facilitate insulin secretion are located in the nucleus ambiguus (NA) and the dorsal motor nucleus of the vagus nerve (DMX). With regard to insulin secretion, hypothalamic (produced by ventromedial hypothalamic (VMH) lesions) and genetic obesities have features in common: (a) insulin oversecretion is an early abnormality in both syndromes; and (b) this abnormality is vagus nerve-mediated. VMH lesions and possible, spontaneously occurring (i.e. genetic) CNS-located abnormalities appear to result in an increased parasympathetic efferent tone together with decreased sympathetic efferent tone that is likely to be responsible for the occurrence of hyperinsulinemia, obesity and, eventually, insulin resistance.

摘要

最终到达胰腺并促进胰岛素分泌的主要脑干副交感传出神经元位于疑核(NA)和迷走神经背运动核(DMX)。关于胰岛素分泌,下丘脑性肥胖(由腹内侧下丘脑(VMH)损伤引起)和遗传性肥胖有共同特征:(a)胰岛素分泌过多是这两种综合征的早期异常;(b)这种异常是由迷走神经介导的。VMH损伤以及可能自发出现的(即遗传性的)中枢神经系统定位异常似乎导致副交感传出神经张力增加,同时交感传出神经张力降低,这可能是导致高胰岛素血症、肥胖以及最终胰岛素抵抗发生的原因。

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