糖毒性下UCP2介导的胰岛功能紊乱的研究  

Islet Dysfunction Mediated by UCP2 under Glucose Toxicity

作　　者：陈莹晖[1,2] 李裕明[2] 邓波[2] 李丽华[2] 高海波[2] 陈璐璐[2] 

机构地区：[1]海南医学院附属医院重症医学科,海口570102 [2]华中科技大学同济医学院附属协和医院内分泌科,武汉430022

出　　处：《华中科技大学学报（医学版）》2010年第2期193-196,共4页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong

摘　　要：目的研究不同浓度高糖对胰岛INS-1细胞解偶联蛋白2(UCP2)基因表达的影响,探讨UCP2基因与高糖刺激下氧化应激和胰岛素分泌之间的关系,进一步了解糖尿病糖毒性的发病机制。方法将不同浓度的葡萄糖作用于INS-1细胞,镜下观察INS-1细胞的形态改变,应用可见分光光度计测定丙二醛(MDA)含量,运用ELISA方法检测葡萄糖刺激的胰岛素分泌(GSIS),同时应用RT-PCR方法检测UCP2基因的表达。结果①随着糖浓度的增加,INS-1细胞的凋亡增多,MDA含量逐渐增加,GSIS值逐渐下降,不同糖浓度组比较,差异具有显著性意义(P<0.01)。②随着葡萄糖浓度增加,INS-1细胞UCP2 mRNA的表达总体逐渐增强。结论高糖可促进INS-1细胞凋亡,在高糖作用下活性氧物质(ROS)代谢产物MDA增多,通过激活UCP2的途径引起胰岛细胞胰岛素分泌功能受损。这可能也是糖毒性对胰岛β细胞损害的一个重要环节。Objective To study the effects of different concentrations of high glucose on uncoupling protein 2（UCP2） gene expression in INS-1 cells and explore the relationships among UCP2 gene and oxidative stress and insulin secretion with high-glucose stimulation in order to further understand the pathogenesis of the high glucose toxicity in diabetes.Methods The INS-1 cells were cultured with different concentrations of high glucose and their morphological changes were observed under an inverted phase contrast microscope.Propanediol（MDA） was determined by spectrophotometer.High glucose-stimulated insulin secretion（GSIS） and UCP2 gene expression were detected by ELESA and RT-PCR,respectively.Results With the elevation in glucose concentration,apoptosis and MDA contents of INS-1 cells were increased,but GSIS decreased（P0.01）.With the elevation in glucose concentration,UCP2 mRNA expression of INS-1 cells was raised gradually.Conclusion The high glucose promotes the apoptosis of INS-1 cells.Under the condition of high glucose,the increase of MDA can impair insulin secretion of islet cells by activating UCP2 pathway,which may be an important part of glucose toxicity in INS-1 cells.

关 键 词：解偶联蛋白2 INS-1细胞 糖毒性 氧化应激 高糖刺激的胰岛素分泌 

分 类 号：R587.1[医药卫生—内分泌]