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胰腺β细胞 KATP 通道:低血糖和高血糖。

Pancreatic β-cell KATP channels: Hypoglycaemia and hyperglycaemia.

机构信息

Developmental Endocrinology Research Group, Clinical and Molecular Genetics Unit, Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.

出版信息

Rev Endocr Metab Disord. 2010 Sep;11(3):157-63. doi: 10.1007/s11154-010-9144-2.

Abstract

The pancreatic β-cell ATP-sensitive K(+) channel (K(ATP) channel) plays a critical role in glucose homeostasis by linking glucose metabolism to electrical excitability and insulin secretion. Changes in the intracellular ratio of ATP/ADP mediate the metabolic regulation of channel activity. The β-cell K(ATP) channel is a hetero-octameric complex composed of two types of subunits: four inward-rectifying potassium channel pore-forming (Kir6.2) subunits and four high-affinity sulfonylurea receptor 1 (SUR1) subunits. Kir6.2 and SUR1 are encoded by the genes KCNJ11 and ABCC8, respectively. Mutations in these genes can result in congenital hyperinsulinism and permanent neonatal diabetes. This review highlights the important role of the β-cell K(ATP) channel in glucose physiology and provides an introduction to some of the other review articles in this special edition of the Reviews in Endocrine and Metabolic Disorders.

摘要

胰岛β细胞 ATP 敏感性钾(KATP)通道在葡萄糖稳态中发挥着关键作用,它将葡萄糖代谢与电兴奋性和胰岛素分泌联系起来。细胞内 ATP/ADP 比值的变化介导了通道活性的代谢调节。β细胞 KATP 通道是一种异源八聚体复合物,由两种类型的亚基组成:四个内向整流钾通道形成(Kir6.2)亚基和四个高亲和力磺酰脲受体 1(SUR1)亚基。Kir6.2 和 SUR1 分别由基因 KCNJ11 和 ABCC8 编码。这些基因的突变可导致先天性高胰岛素血症和永久性新生儿糖尿病。本综述强调了胰岛β细胞 KATP 通道在葡萄糖生理学中的重要作用,并对本刊特刊中其他一些综述文章进行了介绍。

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