Glucose suppresses ATP-inhibited K-channels in pancreatic beta-cells.
Glucose suppresses ATP-inhibited K-channels in pancreatic beta-cells.
复制标题
葡萄糖抑制胰腺 β 细胞中 ATP 抑制的 K 通道。
DOI:
10.1007/978-1-4684-5314-0_5
复制
发表时间:
1986
影响因子:
--
通讯作者:
Satin,LS
中科院分区:
文献类型:
--
作者:
Cook,DL;Hales,CN;Satin,LS
Glucose-induced insulin release involves a cascade of events in the pancreatic β-cell: the metabolism of glucose enhances the net uptake of calcium by the cell, mobilizes calcium from stores within the cell and thus triggers the exocytosis of insulin15. Calcium uptake occurs when glucose depolarizes the β-cell membrane to trigger periodic bursts of calcium action potentials2,3,10,13. The mechanisms which couple glucose metabolism to the depolarization have eluded workers since the late 1960’s. Depolarization is accompanied by increased cell input impedance, decreased dependence of membrane potential on external K+ 2, and decreased efflux of42K+and86Rb+8, all of which depend on glucose metabolism9,12. These findings have suggested the existence of membrane K-channels which are open in low glucose and are closed by a process linked to glucose metabolism. As possibilities, it has been suggested that Ca-activated K-channels are closed by a glucose-induced fall of intracellular free Ca2+ 2, or that K-channels are closed by metabolic proton production and intracellular acidification14.