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首页> 外文期刊>Cell metabolism >Class IA phosphatidylinositol 3-kinase in pancreatic beta cells controls insulin secretion by multiple mechanisms.
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Class IA phosphatidylinositol 3-kinase in pancreatic beta cells controls insulin secretion by multiple mechanisms.

机译：胰腺β细胞中的IA类磷脂酰肌醇3-激酶可通过多种机制控制胰岛素分泌。

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摘要

Type 2 diabetes is characterized by insulin resistance and pancreatic beta cell dysfunction, the latter possibly caused by a defect in insulin signaling in beta cells. Inhibition of class IA phosphatidylinositol 3-kinase (PI3K), using a mouse model lacking the pik3r1 gene specifically in beta cells and the pik3r2 gene systemically (betaDKO mouse), results in glucose intolerance and reduced insulin secretion in response to glucose. beta cells of betaDKO mice had defective exocytosis machinery due to decreased expression of soluble N-ethylmaleimide attachment protein receptor (SNARE) complex proteins and loss of cell-cell synchronization in terms of Ca(2+) influx. These defects were normalized by expression of a constitutively active form of Akt in the islets of betaDKO mice, preserving insulin secretion in response to glucose. The class IA PI3K pathway in beta cells in vivo is important in the regulation of insulin secretion and may be a therapeutic target for type 2 diabetes.
机译：2型糖尿病的特征是胰岛素抵抗和胰腺β细胞功能异常，后者可能是由β细胞中胰岛素信号传导缺陷引起的。使用在模型细胞中缺乏pik3r1基因的小鼠模型和系统性地缺乏pik3r2基因的小鼠模型（betaDKO小鼠），对IA类磷脂酰肌醇3-激酶（PI3K）的抑制会导致葡萄糖耐量下降，并响应于葡萄糖而减少胰岛素分泌。 betaDKO小鼠的beta细胞具有缺陷的胞吐机制，原因是可溶性N-乙基马来酰亚胺附着蛋白受体（SNARE）复杂蛋白的表达降低，并且细胞之间的Ca（2+）流入失去同步。通过在betaDKO小鼠的胰岛中表达Akt的组成型活性形式将这些缺陷归一化，从而保留了对葡萄糖的胰岛素分泌。体内β细胞中的IA类PI3K途径在调节胰岛素分泌中很重要，并且可能是2型糖尿病的治疗靶标。

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