Yoshimoto Y, Fukuyama Y, Horio Y, Inanobe A, Gotoh M, Kurachi Y
Department of Pharmacology II, Faculty of Medicine and Graduate School of Medicine, Osaka University, Suita, Japan.
FEBS Lett. 1999 Feb 12;444(2-3):265-9. doi: 10.1016/s0014-5793(99)00076-9.
Somatostatin inhibits glucagon-secretion from pancreatic alpha cells but its underlying mechanism is unknown. In mouse alpha cells, we found that somatostatin induced prominent hyperpolarization by activating a K+ channel, which was unaffected by tolbutamide but prevented by pre-treating the cells with pertussis toxin. The K+ channel was activated by intracellular GTP (with somatostatin), GTPgammaS or Gbetagamma subunits. It was thus identified as a G protein-gated K+ (K(G)) channel. RT-PCR and immunohistochemical analyses suggested the K(G) channel to be composed of Kir3.2c and Kir3.4. This study identified a novel ionic mechanism involved in somatostatin-inhibition of glucagon-secretion from pancreatic alpha cells.
生长抑素可抑制胰腺α细胞分泌胰高血糖素，但其潜在机制尚不清楚。在小鼠α细胞中，我们发现生长抑素通过激活一种钾离子通道诱导显著的超极化，该通道不受甲苯磺丁脲影响，但用百日咳毒素预处理细胞可将其阻断。该钾离子通道可被细胞内GTP（与生长抑素一起）、GTPγS或Gβγ亚基激活。因此，它被鉴定为一种G蛋白门控钾离子（K(G)）通道。逆转录聚合酶链反应（RT-PCR）和免疫组织化学分析表明，K(G)通道由Kir3.2c和Kir3.4组成。本研究确定了一种参与生长抑素抑制胰腺α细胞分泌胰高血糖素的新离子机制。
