Jacobson D A, Philipson L H
Department of Medicine, The University of Chicago, Chicago, IL 60637, USA.
Diabetes Obes Metab. 2007 Nov;9 Suppl 2(Suppl 2):89-98. doi: 10.1111/j.1463-1326.2007.00784.x.
Coordinated electrical activity allows pancreatic beta-cells to respond to secretagogues with calcium entry followed by insulin secretion. Metabolism of glucose affects multiple membrane proteins including ion channels, transporters and pumps that collaborate in a cascade of electrical activity resulting in insulin release. Glucose induces beta-cell depolarization resulting in the firing of action potentials (APs), which are the primary electrical signal of the beta-cell. They are shaped by orchestrated activation of ion channels. Here we give an overview of the voltage-gated potassium (Kv) channels of the beta-cell, which are responsible in part for the falling phase of the AP, and how their regulation affects insulin secretion. beta cells contain several Kv channels allowing dynamic integration of multiple signals on repolarization of glucose-stimulated APs. Recent studies on Kv channel regulation by cAMP and arachidonic acid and on the Kv2.1 null mouse have greatly increased our understanding of beta-cell excitation-secretion coupling.
协调的电活动使胰腺β细胞能够对促分泌剂作出反应,伴随着钙离子内流,随后分泌胰岛素。葡萄糖代谢会影响多种膜蛋白,包括离子通道、转运体和泵,它们协同作用引发一系列电活动,从而导致胰岛素释放。葡萄糖诱导β细胞去极化,引发动作电位(APs)发放,动作电位是β细胞的主要电信号。它们由离子通道的有序激活形成。在这里,我们概述了β细胞的电压门控钾(Kv)通道,其部分负责动作电位的下降阶段,以及它们的调节如何影响胰岛素分泌。β细胞含有多种Kv通道,可在葡萄糖刺激的动作电位复极化时动态整合多种信号。最近关于环磷酸腺苷(cAMP)和花生四烯酸对Kv通道调节以及Kv2.1基因敲除小鼠的研究,极大地增进了我们对β细胞兴奋-分泌偶联的理解。