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脂肪细胞中GLUT4调节的分子机制。

Molecular mechanisms of GLUT4 regulation in adipocytes.

作者信息

Govers R

机构信息

UMR Inserm U1062, INRA 1260, Aix Marseille University, Campus Timone, Faculty of Medicine, 27, boulevard Jean-Moulin, 13385 Marseille Cedex 5, France.

出版信息

Diabetes Metab. 2014 Dec;40(6):400-10. doi: 10.1016/j.diabet.2014.01.005. Epub 2014 Mar 20.

DOI:10.1016/j.diabet.2014.01.005
PMID:24656589
Abstract

Insulin resistance is strongly linked to type 2 diabetes and associated with a reduced uptake of glucose by muscle and adipose tissue. The transporter that is responsible for this uptake and whose function is disturbed in insulin resistance and type 2 diabetes is GLUT4. In the non-stimulated state, GLUT4 is efficiently sequestered intracellularly. This retention prevents GLUT4 from reaching the cell surface and transporting glucose into muscle and fat cells when blood glucose levels are low. After a meal when blood glucose levels rise, insulin is secreted by the pancreas, which, upon binding to its receptor, triggers an intracellular signaling cascade, leading to the translocation of GLUT4 from intracellular compartments to the cell surface, resulting in glucose uptake and normalization of the blood glucose levels. Its regulation is dominated by its localization, efficient intracellular retention and sensitivity to insulin and contraction, which makes GLUT4 an interesting and unique molecule. These aspects of the intracellular regulation of GLUT4 are described in this review.

摘要

胰岛素抵抗与2型糖尿病密切相关,并与肌肉和脂肪组织对葡萄糖的摄取减少有关。负责这种摄取且其功能在胰岛素抵抗和2型糖尿病中受到干扰的转运蛋白是葡萄糖转运蛋白4(GLUT4)。在非刺激状态下,GLUT4有效地被隔离在细胞内。这种保留阻止了GLUT4在血糖水平低时到达细胞表面并将葡萄糖转运到肌肉和脂肪细胞中。进食后血糖水平升高时,胰腺分泌胰岛素,胰岛素与其受体结合后触发细胞内信号级联反应,导致GLUT4从细胞内区室转运到细胞表面,从而实现葡萄糖摄取并使血糖水平恢复正常。其调节主要由其定位、有效的细胞内保留以及对胰岛素和收缩的敏感性决定,这使得GLUT4成为一个有趣且独特的分子。本文综述了GLUT4细胞内调节的这些方面。

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