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首页> 外文期刊>Cell metabolism >Glucose recruits K(ATP) channels via non-insulin-containing dense-core granules.
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Glucose recruits K(ATP) channels via non-insulin-containing dense-core granules.

机译：葡萄糖通过不含胰岛素的致密颗粒吸收K（ATP）通道。

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摘要

beta cells rely on adenosine triphosphate-sensitive potassium (K(ATP)) channels to initiate and end glucose-stimulated insulin secretion through changes in membrane potential. These channels may also act as a constituent of the exocytotic machinery to mediate insulin release independent of their electrical function. However, the molecular mechanisms whereby the beta cell plasma membrane maintains an appropriate number of K(ATP) channels are not known. We now show that glucose increases K(ATP) current amplitude by increasing the number of K(ATP) channels in the beta cell plasma membrane. The effect was blocked by inhibition of protein kinase A (PKA) as well as by depletion of extracellular or intracellular Ca(2+). Furthermore, glucose promoted recruitment of the potassium inward rectifier 6.2 to the plasma membrane, and intracellular K(ATP) channels localized in chromogranin-positive/insulin-negative dense-core granules. Our data suggest that glucose can recruit K(ATP) channels to the beta cell plasma membrane via non-insulin-containing dense-core granules in a Ca(2+)- and PKA-dependent manner.
机译：β细胞依靠三磷酸腺苷敏感性钾（K（ATP））通道通过膜电位的变化来启动和终止葡萄糖刺激的胰岛素分泌。这些通道还可以充当胞吐机制的成分，以独立于其电功能介导胰岛素释放。但是，β细胞质膜维持适当数量的K（ATP）通道的分子机制尚不清楚。我们现在显示葡萄糖通过增加β细胞质膜中K（ATP）通道的数量来增加K（ATP）电流幅度。通过抑制蛋白激酶A（PKA）以及通过消耗细胞外或细胞内Ca（2+）来阻止这种作用。此外，葡萄糖促进钾内向整流子6.2募集到质膜，以及细胞内K（ATP）通道位于嗜铬粒蛋白阳性/胰岛素阴性致密颗粒中。我们的数据表明，葡萄糖可以通过不包含胰岛素的致密颗粒以Ca（2+）和PKA依赖性方式募集K（ATP）通道至β细胞质膜。

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