R6/2型亨廷顿病转基因小鼠胰岛β细胞功能损伤  

Impaired function of pancreatic β cells in the R6/2 transgenic mouse model of Huntington's disease

作　　者：叶翠芳[1] 李和[1] 

机构地区：[1]华中科技大学同济医学院解剖学系组织胚胎学教研室,教育部神经系统疾病重点实验室,湖北武汉430030

出　　处：《中国病理生理杂志》2009年第7期1386-1389,共4页Chinese Journal of Pathophysiology

基　　金：国家杰出青年科学基金资助项目(No.30225024)

摘　　要：目的:研究R6/2型亨廷顿病(HD)转基因小鼠胰岛β细胞的功能,揭示HD转基因小鼠继发糖尿病的机制。方法:利用R6/2型HD转基因小鼠模型,检测正常和HD小鼠空腹血糖以及血清胰岛素水平;并应用HE染色和免疫荧光技术分析正常和HD小鼠胰岛形态学差异。结果:与正常小鼠相比,R6/2型HD小鼠空腹血糖显著增高,血清胰岛素水平明显降低,胰岛萎缩,β细胞数量减少,细胞功能指数降低,而胰岛素抵抗指数正常。结论:胰岛β细胞功能损伤是引起R6/2HD转基因小鼠继发糖尿病发生的主要因素。AIM ： To study the function of pancreatic β cells in the R6/2 transgenic mouse of Huntington＇s disease（ HD）, and to elucidate the pathogenetic mechanisms underlying diabetes mellitus in transgenic mice of HD. METHODS ： By using the R6/2 transgenic mouse model of HD, fasting blood glucose and fasting insulin concentration in plasma of normal and HD mice were detected. Further, HE staining and immunofluorescence technique were used for morphometric analysis of islets in normal and HD mice. RESULTS： In contrast to normal mouse, R6/2 HD mouse showed hyperglycemia and hypoinsulinemia in fasting state. Pancreatic islets morphology showed that islets atrophied and cell number decreased in HD mouse. Poor functional index was observed in these mice, but insulin resistance index was normal. CONCLUSION： Impaired function of pancreatic cells may be the key factor contributing to the pathogenesis of diabetes in the R6/2 trans- genic mouse model of HD.

关 键 词：亨廷顿病 糖尿病 胰腺Β细胞 R6/2小鼠 

分 类 号：R363[医药卫生—病理学]