Stop signs in hippocampal insulin signaling: the role of insulin resistance in structural, functional and behavioral deficits.
Stop signs in hippocampal insulin signaling: the role of insulin resistance in structural, functional and behavioral deficits.
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DOI：
10.1016/j.cobeha.2015.12.004
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发表时间：
2016-06-01
影响因子：
5
通讯作者：
Reagan LP
中科院分区：
文献类型：
--
作者：
Fadel JR;Reagan LP
在外周组织中，胰岛素激活信号级联反应，促进葡萄糖从血液中摄取到肝脏、肌肉和脂肪等组织。虽然胰岛素似乎在中枢神经系统（CNS）的葡萄糖摄取调节中起次要作用，但已知胰岛素在调节海马等大脑区域的突触可塑性方面起主要作用。胰岛素调节海马神经可塑性的概念得到了2型糖尿病（T2DM）和阿尔茨海默病（AD）动物模型的进一步支持。本综述的目的是提供这些研究的概述，以及研究海马胰岛素信号缺陷是否适用于干预策略。
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.