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首页> 外文期刊>Endocrinology >Impaired insulin exocytosis in neural cell adhesion molecule-/- mice due to defective reorganization of the submembrane F-actin network.
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Impaired insulin exocytosis in neural cell adhesion molecule-/- mice due to defective reorganization of the submembrane F-actin network.

机译：神经细胞粘附分子中的胰岛素外尿量受损 - / - 由于底膜F型肌动蛋白网络的重组缺陷。

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The neural cell adhesion molecule (NCAM) is required for cell type segregation during pancreatic islet organogenesis. We have investigated the functional consequences of ablating NCAM on pancreatic beta-cell function. In vivo, NCAM(-/-) mice exhibit impaired glucose tolerance and basal hyperinsulinemia. Insulin secretion from isolated NCAM(-/-) islets is enhanced at glucose concentrations below 15 mM but inhibited at higher concentrations. Glucagon secretion from pancreatic alpha-cells evoked by low glucose was also severely impaired in NCAM(-/-) islets. The diminution of insulin secretion is not attributable to defective glucose metabolism or glucose sensing (documented as glucose-induced changes in intracellular Ca(2+) and K(ATP)-channel activity). Resting K(ATP) conductance was lower in NCAM(-/-) beta-cells than wild-type cells, and this difference was abolished when F-actin was disrupted by cytochalasin D (1 muM). In wild-type beta-cells, the submembrane actin network disassembles within 10 min during glucose stimulation (30 mM), an effect not seen in NCAM(-/-) beta-cells. Cytochalasin D eliminated this difference and normalized insulin and glucagon secretion in NCAM(-/-) islets. Capacitance measurements of exocytosis indicate that replenishment of the readily releasable granule pool is suppressed in NCAM(-/-) alpha- and beta-cells. Our data suggest that remodeling of the submembrane actin network is critical to normal glucose regulation of both insulin and glucagon secretion.
机译：在胰岛素发生期间，细胞型偏析需要神经细胞粘附分子（NCAM）。我们研究了消融NCAM在胰腺β细胞功能上的功能后果。体内，NCAM（ - / - ）小鼠表现出葡萄糖耐受性和基础胰岛素血症的损伤。来自分离的NCAM（ - / - ）胰岛的胰岛素分泌在低于15mm以下的葡萄糖浓度下增强但在较高浓度下抑制。从低葡萄糖引起的胰腺α细胞的胰高血糖素分泌物在NCAM（ - / - ）胰岛中也受到严重受损。胰岛素分泌的减少不归因于葡萄糖代谢或葡萄糖感测（记录为细胞内Ca（2+）和K（ATP）-Channel活性的葡萄糖诱导的变化）。在NCAM（ - / - ）β细胞中静止k（ATP）电导比野生型细胞低，并且当F-actin被细胞蛋白D（1妈妈）破坏时，废除这种差异。在野生型β细胞中，膜肌动蛋白网络在葡萄糖刺激（30mm）期间在10分钟内拆卸，在NCAM（ - / - ）β细胞中未见的效果。细胞蛋白D消除了NCAM（ - / - ）胰岛中的这种差异和标准化的胰岛素和胰高血糖素分泌。外卵瘤的电容测量表明，在NCAM（ - / - ）α-和β细胞中抑制了易释放的颗粒池的补充。我们的数据表明，蒙膜肌动蛋白网络的重塑对于胰岛素和胰高血糖素分泌的正常葡萄糖调节至关重要。

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