Swelling of secretory vesicles is critical for the regulated release of intra-vesicular contents from cells during secretion. At the secretory vesicle membrane of the exocrine pancreas and neurons, GTP-binding G proteins, vH+-ATPase, potassium channels and AQP water channels, are among the players implicated in vesicle volume regulation. Here we report in the endocrine insulin-secreting MIN6 cells, the similar requirement of vH+-ATPase-mediated intracellular acidification on glucose-stimulated insulin release. MIN6 cells exposed to the vH+-ATPase inhibitor Bafilomycin A show decreased acidification of the cytosolic compartment that include insulin-carrying granules. Additionally, a loss of insulin granules near the cell plasma membrane following Bafilomycin A treatment, suggests impaired transport of insulin granules and consequent decrease in glucose-stimulated insulin secretion and accumulation of intracellular insulin. These results suggest that vH+-ATPase-mediated intracellular acidification is required for insulin secretion in beta cells.

中文翻译：

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vH + -ATPase诱导的细胞内酸化对于葡萄糖刺激β细胞中的胰岛素分泌至关重要。

分泌囊泡的膨胀对于分泌过程中细胞内囊泡内容物的调节释放至关重要。在外分泌胰腺和神经元的分泌性囊泡膜上，与GTP结合的G蛋白，vH + -ATPase，钾通道和AQP水通道参与了囊泡体积调节。在这里，我们报道了在分泌内分泌胰岛素的MIN6细胞中，vH + -ATPase介导的细胞内酸化对葡萄糖刺激的胰岛素释放的相似要求。暴露于vH + -ATPase抑制剂Bafilomycin A的MIN6细胞显示胞质区的酸化降低，其中包括携带胰岛素的颗粒。此外，Bafilomycin A处理后，细胞质膜附近的胰岛素颗粒丢失，提示胰岛素颗粒的运输受损，并因此降低了葡萄糖刺激的胰岛素分泌和细胞内胰岛素的积累。这些结果表明，vH + -ATPase介导的细胞内酸化是β细胞中胰岛素分泌所必需的。