GLUCOSE INDUCES CLOSURE OF SINGLE POTASSIUM CHANNELS IN ISOLATED RAT PANCREATIC BETA-CELLS
GLUCOSE INDUCES CLOSURE OF SINGLE POTASSIUM CHANNELS IN ISOLATED RAT PANCREATIC BETA-CELLS
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DOI：
10.1038/312446a0
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发表时间：
1984-01-01
期刊：
影响因子：
64.8
通讯作者：
ASHCROFT, SJH
中科院分区：
文献类型：
--
作者：
ASHCROFT, FM;HARRISON, DE;ASHCROFT, SJH
从胰腺β细胞分泌胰岛素的主要生理刺激是血浆葡萄糖浓度的增加。已经确定，葡萄糖刺激的胰岛素分泌与β细胞中电活动的出现相关1，2;高于胰岛素释放阈值水平的葡萄糖浓度产生缓慢的膜去极化，随后是动作电位的振荡爆发（5-15 mM葡萄糖）或连续尖峰（> 16 mM葡萄糖）。示踪剂通量研究3和使用完整胰岛4的微电极测量表明，葡萄糖诱导的初始去极化是由静息膜对钾的渗透性降低引起的。证据还表明，对葡萄糖的电反应5、离子反应6和分泌反应7，8是由β细胞内糖的代谢介导的。通过使用来自分离的大鼠胰腺β细胞的细胞附着膜贴片9，我们现在已经确定了一种钾通道（G通道），该通道在静息电位下是活跃的，并被葡萄糖抑制。该通道的关闭需要葡萄糖代谢。这是第一个报告的钾通道，其活动是由葡萄糖调节，并可能耦合参与胰岛素分泌的代谢和离子事件。
The major physiological stimulus for the secretion of insulin from the pancreaticβ-cell is an increase in the plasma glucose concentration. It is well established that glucose-stimulated insulin secretion is associated with the appearance of electrical activity in theβ-cell1,2; glucose concentrations above the threshold level for insulin release produce a slow membrane depolarization followed by either oscillatory bursts of action potentials (5–15 mM glucose) or continuous spiking (>16mM glucose). Tracer flux studies3and microelectrode measurements using intact islets of Langerhans4have indicated that the initial depolarization induced by glucose is caused by a decrease in the resting membrane permeability to potassium. Evidence also suggests that the electrical5, ionic6and secretory responses7,8to glucose are mediated by the metabolism of the sugar within theβ-cell. By using cell-attached membrane patches9from isolated rat pancreaticβ-cells, we have now identified a potassium channel (G-channel) that is active at the resting potential and is inhibited by glucose. Closure of this channel requires glucose metabolism. This is the first report of a potassium channel whose activity is modulated by glucose, and which may couple metabolic and ionic events involved in the secretion of insulin.