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电压依赖性钾通道的抑制介导大鼠胰腺β细胞中cAMP增强的胰岛素分泌。

Inhibition of voltage-dependent potassium channels mediates cAMP-potentiated insulin secretion in rat pancreatic β cells.

作者信息

Liu Yunfeng, Zhong Xiangqin, Ding Yaqin, Ren Lele, Bai Tao, Liu Mengmeng, Liu Zhihong, Guo Yangyan, Guo Qing, Zhang Yu, Yang Jing, Zhang Yi

机构信息

a Department of Endocrinology , the First Hospital of Shanxi Medical University, Shanxi Medical University , Taiyuan , China.

b Department of Pharmacology , Shanxi Medical University , Taiyuan , China.

出版信息

Islets. 2017 Mar 4;9(2):11-18. doi: 10.1080/19382014.2017.1280644. Epub 2017 Jan 19.

Abstract

Insulin secretion is essential for maintenance of glucose homeostasis. An important intracellular signal regulating insulin secretion is cAMP. In this report, we showed that an increase of cAMP induced by adenylyl cyclase (AC) activator forskolin or by cAMP analog db-cAMP not only potentiated insulin secretion but also inhibited Kv channels, and these effects were reversed by AC inhibitor SQ22536. The cAMP-mediated Kv channel inhibition resulted in prolongation of action potential duration, which partly accounts for the elevation of intracellular Ca induced by activation of cAMP signaling. Taken together, the results suggest that Kv channels are involved in cAMP-potentiated insulin secretion in pancreatic β cells.

摘要

胰岛素分泌对于维持葡萄糖稳态至关重要。调节胰岛素分泌的一个重要细胞内信号是环磷酸腺苷(cAMP)。在本报告中,我们表明,由腺苷酸环化酶(AC)激活剂福斯高林或cAMP类似物双丁酰环磷腺苷(db-cAMP)诱导的cAMP增加不仅增强了胰岛素分泌,还抑制了钾离子通道(Kv通道),并且这些作用被AC抑制剂SQ22536逆转。cAMP介导的Kv通道抑制导致动作电位持续时间延长,这部分解释了cAMP信号激活所诱导的细胞内钙离子升高。综上所述,结果表明Kv通道参与胰腺β细胞中cAMP增强的胰岛素分泌。

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