摘要
目的:通过比较肝脏特异性葡萄糖激酶基因敲除小鼠和两种链脲菌素诱导的糖尿病小鼠模型血清肿瘤坏死因子α(TNFα)水平,初步探讨TNFα在糖尿病发病过程中的作用。方法:建立n49-STZ小鼠模型、n5-STZ小鼠模型和肝脏特异性葡萄糖激酶基因敲除小鼠模型,分别检测各种模型小鼠空腹血糖、血清胰岛素和TNFα水平;并对各组肝脏、胰腺、心脏和肌肉组织进行形态学分析。结果:各种模型小鼠空腹血糖值均显著高于正常小鼠;n5-STZ小鼠模型血清胰岛素和TNFα水平明显高于正常对照组;n49-STZ小鼠模型血清胰岛素水平显著低于正常小鼠;其余模型小鼠血TNFα水平有增高的趋势;n49-STZ和n5-STZ小鼠模型均出现胰岛萎缩和肝小叶条索紊乱的现象。结论:n5-STZ糖尿病小鼠模型中血清TNFα水平增高的变化提示TNFα可能在糖尿病发病过程中起着重要的作用。
AIM： To compare serum tumor necrosis factor α （TNFα） concentration in liver specific glucokinase gene knockout mice and two kinds of streptozotocin induced diabetic mice, and to explore the possible role of TNFα in the pathogenesis of diabetes mellitus. METHODS： Firstly three kinds of diabetic animal models were generated including n49-STZ mouse model, nS-STZ mouse model and liver specific glucokinase gene knockout mouse model. Then fasting blood glucose, serum insulin and TNFα concentrations were determined. Morphology analysis was conducted on sections of pancreas, liver, heart and muscle. RESULTS： Fasting blood glucose levels were significantly elevated in all the three kinds of diabetic mice models compared with normal controls. Only nS-STZ mouse model showed significantly higher serum insulin and TNFα concentrations than the controls, but serum insulin levels were significantly lowered in n49-STZ mouse model, serum TNFα concentration in n49-STZ mouse model and glucokinase gene knockout mouse model had the propensity to increase. Morphology analysis of sections from n49-STZ and nS-STZ mice showed pancreatic islets atrophy and disordered hepatic lobule cables. CONCLUSION： Alteration in serum TNFα concentration of the diabetic mice models implicated that TNFα play an important role in the pathogenesis of diabetes mellitus.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2006年第7期735-738,共4页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
中国高技术研究发展计划(863计划)资助(№108208208203№2002AA214201)
