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首页> 外文期刊>Cell metabolism >CAPS1 and CAPS2 regulate stability and recruitment of insulin granules in mouse pancreatic beta cells.
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CAPS1 and CAPS2 regulate stability and recruitment of insulin granules in mouse pancreatic beta cells.

机译：CAPS1和CAPS2调节小鼠胰腺β细胞中胰岛素颗粒的稳定性和募集。

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摘要

CAPS1 and CAPS2 regulate dense-core vesicle release of transmitters and hormones in neuroendocrine cells, but their precise roles in the secretory process remain enigmatic. Here we show that CAPS2(-/-) and CAPS1(+/-);CAPS2(-/-) mice, despite having increased insulin sensitivity, are glucose intolerant and that this effect is attributable to a marked reduction of glucose-induced insulin secretion. This correlates with diminished Ca(2+)-dependent exocytosis, a reduction in the size of the morphologically docked pool, a decrease in the readily releasable pool of secretory vesicles, slowed granule priming, and suppression of second-phase (but not first-phase) insulin secretion. In beta cells of CAPS1(+/-);CAPS2(-/-) mice, the lowered insulin content and granule numbers were associated with an increase in lysosome numbers and lysosomal enzyme activity. We conclude that although CAPS proteins are not required for Ca(2+)-dependent exocytosis to proceed, they exert a modulatory effect on insulin granule priming, exocytosis, and stability.
机译：CAPS1和CAPS2调节神经内分泌细胞中递质和激素的密实小泡释放，但它们在分泌过程中的确切作用仍然是个谜。在这里，我们显示CAPS2（-/-）和CAPS1（+/-）; CAPS2（-/-）小鼠尽管胰岛素敏感性增强，但对葡萄糖不耐受，并且这种作用可归因于葡萄糖诱导的胰岛素的明显减少分泌。这与减少的Ca（2+）依赖的胞吐作用，形态停靠的池大小的减少，分泌囊泡的易于释放池的减少，颗粒引发的放慢和第二阶段的抑制（但不是第一阶段）相关。期）胰岛素分泌。在CAPS1（+/-）; CAPS2（-/-）小鼠的β细胞中，降低的胰岛素含量和颗粒数与溶酶体数和溶酶体酶活性的增加有关。我们得出结论，尽管CAPS蛋白不是进行Ca（2+）依赖的胞吐作用所必需的，但它们对胰岛素颗粒引发，胞吐作用和稳定性发挥调节作用。

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