Ashcroft Frances M
Henry Wellcome Centre for Gene Function, Dept. of Physiology, Anatomy and Genetics, Univ. of Oxford, Parks Road, Oxford OX1 3PT, UK.
Am J Physiol Endocrinol Metab. 2007 Oct;293(4):E880-9. doi: 10.1152/ajpendo.00348.2007. Epub 2007 Jul 24.
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.
本文基于一篇为纪念内环境稳态倡导者沃尔特·B·坎农而在美国生理学会发表的演讲。它聚焦于ATP敏感性钾离子（K(ATP)）通道在葡萄糖稳态中的作用，尤其关注其在胰腺β细胞胰岛素分泌中的作用。β细胞K(ATP)通道由形成孔道的Kir6.2和调节性SUR1亚基组成，任一类型亚基的突变都可能导致胰岛素释放过少或过多。在此，我回顾了关于K(ATP)通道结构与功能关系的最新信息，并探讨了K(ATP)通道基因突变如何导致新生儿糖尿病或先天性高胰岛素血症。
