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脂肪细胞中胰岛素刺激葡萄糖摄取的分子机制。

Molecular mechanisms of insulin-stimulated glucose uptake in adipocytes.

作者信息

Ducluzeau P-H, Fletcher L M, Vidal H, Laville M, Tavaré J M

机构信息

Department of Biochemistry, School of Medical Sciences, University of Bristol, BS8 1TD, UK.

出版信息

Diabetes Metab. 2002 Apr;28(2):85-92.

Abstract

The stimulation of muscle and adipose tissue glucose metabolism, which is ultimately responsible for bringing about post-absorptive blood glucose clearance, is the primary clinically relevant action of insulin. Insulin acts on many steps of glucose metabolism, but one of the most important effects is its ability to increase the rate of cellular glucose transport. This results from the translocation of the insulin-responsive transporter isoform, GLUT4, from intra-cellular vesicular storage sites to the plasma membrane. In adipocytes, a substantial amount of cellular GLUT4 is located in a specific highly insulin-responsive storage pool, termed GLUT4 Storage Vesicles (GSVs). GLUT4 can also translocate to the plasma membrane from the recycling endosomal pool which also additionally contains the GLUT1 isoform of glucose transporter and the transferrin receptor. In this article we review the molecular mechanism by which insulin stimulates GLUT4 translocation in adipose cells, including the nature of the signaling pathways involved and the role of the cytoskeleton.

摘要

刺激肌肉和脂肪组织的葡萄糖代谢,这最终负责实现吸收后血糖清除,是胰岛素主要的临床相关作用。胰岛素作用于葡萄糖代谢的多个步骤,但最重要的作用之一是其增加细胞葡萄糖转运速率的能力。这是由于胰岛素反应性转运异构体GLUT4从细胞内囊泡储存位点转运到质膜所致。在脂肪细胞中,大量细胞GLUT4位于特定的高度胰岛素反应性储存池中,称为GLUT4储存囊泡(GSV)。GLUT4也可以从回收内体池中转运到质膜,回收内体池还额外包含葡萄糖转运体的GLUT1异构体和转铁蛋白受体。在本文中,我们综述了胰岛素刺激脂肪细胞中GLUT4转运的分子机制,包括所涉及的信号通路的性质以及细胞骨架的作用。

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