LRP16基因通过上调GLUT-2促进MIN6细胞胰岛素分泌
LRP16 gene increases insulin secretion by up-regulating GLUT-2 in MIN6 cell line
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摘要: 目的: 探讨LRP16基因对MIN6细胞葡萄糖刺激胰岛素分泌的影响及其可能机制。方法: 用Super-Fect脂质体转染法建立稳定过表达LRP16基因的MIN6细胞株,以转染空质粒的MIN6细胞株作为对照。检测两组细胞的增殖、胰岛素分泌及GLUT-2蛋白的表达情况。结果: 过表达组的增殖与对照组相比无显著差别(P>0.05);在0mmol/L、3mmol/L、30mmol/L葡萄糖刺激下,过表达组的胰岛素分泌量分别为对照组的2.26倍、2.19倍和2.16倍(P<0.05);westernblot显示过表达组GLUT-2蛋白量比对照组显著上调(P<0.05)。结论: 过表达LRP16基因不能促进MIN6细胞增殖,但可以通过上调GLUT-2促进胰岛素分泌。表明LRP16基因促进胰岛素分泌的作用不依赖细胞增殖,而依赖细胞对葡萄糖摄取的增加。Abstract: Objective: To explore the effects of LRP16 gene on glucose-stimulated insulin secretion(GSIS)and the possible mechanism in MIN6 cell line. Methods: Stable overexpression of LRP16 cell models was established by SuperFect strategy.The effects of LRP16 overexpression on MIN6 cell proliferation were examined by MTT method.Different concentrations of glucose were used to evaluate the effects of GSIS in the transfected cells.The expression levels of GLUT-2 in MIN6 cells were analysed by western blot. Results: Overexpression of LRP16 did not improve cell proliferation compared with control group(P>0.05),but it increased GSIS by 2.26,2.19 and 2.16 folds under 0mmol/L,3mmol/L and 30mmol/L glucose concentrations respectively,and western blot analyses showed that the levels of GLUT-2 in LRP16 overexpression group increased significantly compared with control group(P<0.05). Conclusion: Overexpression of LRP16 can not improve cell proliferation,but it can increase GSIS by up-regulating GLUT-2 in MIN6 cell line(P<0.05).This may indicate that the effects of LRP16 on GSIS do not rely on cell proliferation but on increased uptake of glucose.
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