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应激、抑郁与糖尿病的神经内分泌联系。

Neuroendocrine link between stress, depression and diabetes.

机构信息

Department of Experimental Neuroendocrinology, Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, PL 31-343 Kraków, Poland.

出版信息

Pharmacol Rep. 2013;65(6):1591-600. doi: 10.1016/s1734-1140(13)71520-2.

Abstract

Clinical studies have indicated a frequent coexistence of depression and diabetes. Both of these diseases are associated with similar changes in the structure and function of the central nervous system cells and with similar disturbances of cognitive processes. Some morphological and functional changes occurring in these diseases seem to result from exaggerated glucocorticoid, proinflammatory cytokine or glutamate action. Glucocorticoids induced by stress are known not only to affect synaptic plasticity but also to disturb brain glucose metabolism and decrease insulin sensitivity. Functional neuroimaging studies demonstrated altered glucose metabolism in the brains of depressed patients. Changes in the amount or activity of key metabolic enzymes and a lower sensitivity of insulin receptors have been detected in the brains of animal models of both of these diseases. Hence, excess glucocorticoids can lead to impaired insulin action and glucose metabolism, to limited energy supply for proper neuronal function and, consequently, to disturbed synaptic plasticity.

摘要

临床研究表明,抑郁和糖尿病经常同时存在。这两种疾病都与中枢神经系统细胞的结构和功能的相似变化以及认知过程的相似障碍有关。这些疾病中发生的一些形态和功能变化似乎是由于糖皮质激素、促炎细胞因子或谷氨酸作用的过度增强所致。应激引起的糖皮质激素不仅会影响突触可塑性,还会干扰大脑葡萄糖代谢并降低胰岛素敏感性。功能神经影像学研究表明,抑郁患者的大脑葡萄糖代谢发生改变。在这两种疾病的动物模型中,已经检测到关键代谢酶的数量或活性的变化以及胰岛素受体的敏感性降低。因此,过量的糖皮质激素可导致胰岛素作用和葡萄糖代谢受损,导致适当神经元功能的能量供应有限,从而导致突触可塑性紊乱。

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