ATP-sensitive K+ channels and disease:: from molecule to malady

被引：88

作者：

Ashcroft, Frances M.

机构：

[1] Univ Oxford, Dept Physiol Anat & Genet, Ctr Gene Funct, Oxford OX1 3PT, England

[2] Univ Oxford, Henry Wellcome Ctr Gene Fucnt, Oxford OX1 2JD, England

来源：

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM | 2007年 / 293卷 / 04期

基金：

英国惠康基金;

关键词：

Kir6.2; SUR1; neonatal diabetes; hyperinsulinism;

D O I：

10.1152/ajpendo.00348.2007

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

This essay is based on a lecture given to the American Physiological Society in honor of Walter B. Cannon, an advocate of homeostasis. It focuses on the role of the ATP-sensitive potassium K+ (K-ATP) channel in glucose homeostasis and, in particular, on its role in insulin secretion from pancreatic beta-cells. The beta-cell K-ATP channel comprises pore-forming Kir6.2 and regulatory SUR1 subunits, and mutations in either type of subunit can result in too little or too much insulin release. Here, I review the latest information on the relationship between K-ATP channel structure and function, and consider how mutations in the K-ATP channel genes lead to neonatal diabetes or congenital hyperinsulinism.

引用

页码：E880 / E889

页数：10

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