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海马体胰岛素信号通路中的“停止信号”:胰岛素抵抗在结构、功能及行为缺陷中的作用

Stop signs in hippocampal insulin signaling: the role of insulin resistance in structural, functional and behavioral deficits.

作者信息

Fadel Jim R, Reagan Lawrence P

机构信息

Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine, Columbia, SC, USA.

Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine, Columbia, SC, USA; WJB Dorn Veterans Affairs Medical Center, Columbia, SC, USA.

出版信息

Curr Opin Behav Sci. 2016 Jun 1;9:47-54. doi: 10.1016/j.cobeha.2015.12.004. Epub 2015 Dec 1.

Abstract

In peripheral tissues insulin activates signaling cascades to facilitate glucose uptake from the blood into tissues like liver, muscle and fat. While insulin appears to play a minor role in the regulation of glucose uptake in the central nervous system (CNS), insulin is known to play a major role in regulating synaptic plasticity in brain regions like the hippocampus. The concept that insulin regulates hippocampal neuroplasticity is further supported from animal models of type 2 diabetes (T2DM) and Alzheimer's disease (AD). The goal of this review is to provide an overview of these studies, as well as the studies that have examined whether deficits in hippocampal insulin signaling are amenable to intervention strategies.

摘要

在周围组织中,胰岛素激活信号级联反应,以促进血液中的葡萄糖摄取到肝脏、肌肉和脂肪等组织中。虽然胰岛素在中枢神经系统(CNS)的葡萄糖摄取调节中似乎起次要作用,但已知胰岛素在调节海马体等脑区的突触可塑性方面起主要作用。2型糖尿病(T2DM)和阿尔茨海默病(AD)的动物模型进一步支持了胰岛素调节海马体神经可塑性的概念。本综述的目的是概述这些研究,以及那些研究了海马体胰岛素信号缺陷是否适合干预策略的研究。

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