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首页> 外文期刊>Cell metabolism >Kv2.1 ablation alters glucose-induced islet electrical activity, enhancing insulin secretion.
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Kv2.1 ablation alters glucose-induced islet electrical activity, enhancing insulin secretion.

机译：Kv2.1消融改变葡萄糖诱导的胰岛电活动，增强胰岛素分泌。

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摘要

Voltage-gated potassium currents (Kv), primarily due to Kv2.1 channels, are activated by glucose-stimulated pancreatic beta cell depolarization, but the exact role (or roles) of this channel in regulating insulin secretion remains uncertain. Here we report that, compared with controls, Kv2.1 null mice have reduced fasting blood glucose levels and elevated serum insulin levels. Glucose tolerance is improved and insulin secretion is enhanced compared to control animals, with similar results in isolated islets in vitro. Isolated Kv2.1(-/-) beta cells have residual Kv currents, which are decreased by 83% at +50 mV compared with control cells. The glucose-induced action potential (AP) duration is increased while the firing frequency is diminished, similar to the effect of specific toxins on control cells but substantially different from the effect of the less specific blocker tetraethylammonium. These results reveal the specific role of Kv2.1 in modulating glucose-stimulated APs of beta cells, exposing additional important currents involved in regulating physiological insulin secretion.
机译：电压门控钾电流（Kv）主要归因于Kv2.1通道，由葡萄糖刺激的胰岛β细胞去极化激活，但该通道在调节胰岛素分泌中的确切作用（或多种作用）仍不确定。在这里，我们报告与对照组相比，空Kv2.1小鼠的空腹血糖水平降低，血清胰岛素水平升高。与对照动物相比，葡萄糖耐受性得到改善，胰岛素分泌得到增强，在离体的胰岛中获得相似的结果。分离的Kv2.1（-/-）β细胞具有残余Kv电流，与对照细胞相比，在+50 mV时，其Kv电流降低了83％。葡萄糖诱导的动作电位（AP）持续时间增加，击发频率降低，这与特定毒素对对照细胞的作用相似，但与特异性较低的阻断剂四乙铵的作用实质上不同。这些结果揭示了Kv2.1在调节葡萄糖刺激的β细胞AP中的特定作用，从而暴露了涉及调节生理胰岛素分泌的其他重要电流。

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