Autocrine anti-apoptotic and proliferative effects of insulin in pancreatic β-cells
Autocrine anti-apoptotic and proliferative effects of insulin in pancreatic β-cells
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DOI：
10.1016/j.febslet.2006.11.066
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发表时间：
2006-12-22
期刊：
影响因子：
3.5
通讯作者：
Persaud, Shanta J.
中科院分区：
文献类型：
--
作者：
Muller, Dany;Jones, Peter M.;Persaud, Shanta J.
胰岛素和葡萄糖可抑制MIN6胰岛素分泌细胞系的凋亡。25 mM葡萄糖的保护作用可被抗胰岛素抗体阻止，而这种抗体诱导的细胞凋亡增加可被过量胰岛素的存在所逆转。葡萄糖刺激MIN6细胞增殖，这一作用可被胰岛素分泌阻断、抗胰岛素抗体和磷脂酰肌醇-3激酶(PI-3K)抑制。此外，去极化浓度的KCI和胰岛素本身也能刺激MIN6细胞的增殖。这些数据表明，胰岛β细胞在血糖升高时分泌的胰岛素具有自分泌作用，从而保护细胞免于凋亡和刺激增殖，并提示胰岛素信号通路通过PI-3K通路可能是维持糖尿病患者胰岛β细胞质量的有效手段。(C)2006年欧洲生化学会联合会。爱思唯尔出版，版权所有。
Insulin and glucose inhibited apoptosis in the MIN6 insulin-secreting cell line. The protective effect of 25 mM glucose was prevented by an anti-insulin antibody and this antibodyinduced increase in apoptosis was reversed by the presence of excess insulin. Glucose stimulated MIN6 cell proliferation and this was inhibited by blockade of insulin secretion, by an anti-insulin antibody and by phosphatidylinositol-3 kinase (PI-3K) inhibition. Furthermore, MIN6 cell proliferation was stimulated by depolarising concentrations of KCI and by insulin itself. These data indicate that insulin secreted by beta-cells in response to elevated glucose exerts autocrine effects to protect against apoptosis and stimulate proliferation, and suggest that the insulin signalling cascade, through the PI-3K pathway, may be an effective means of maintaining beta-cell mass in diabetes. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.