目的 运用高热量高蛋白饮食诱导GK大鼠2型糖尿病肾病模型的建立,并探讨其可能的作用机制.方法 28周龄GK大鼠24只,随机分成对照组、模型组,每组各12只,模型组给予高热量高蛋白饮食,对照组给予正常饮食,共8周.于第0、4、8周观察24 h尿微量白蛋白、24h尿蛋白、尿肌酐、尿微量白蛋白/尿肌酐比值水平；于第0、8周观察空腹血糖和血清肌酐、尿素氮、总胆固醇、甘油三脂、一氧化氮水平；实验结束时取双肾称重并计算肾肥大指数,取肾组织观察病理形态学变化,检测肾组织钠钾ATP酶活性.结果 与对照组比,模型组大鼠24 h尿微量白蛋白、24 h尿蛋白、尿微量白蛋白/尿肌酐比值、空腹血糖、总胆固醇、甘油三脂、一氧化氮、肾肥大指数水平和肾组织钠钾ATP酶活性显著提高,模型组肾小球体积增大,系膜基质增生,基底膜增厚明显.结论 运用高热量高蛋白饮食诱导GK大鼠可成功建立2型糖尿病肾病模型.血糖血脂的上升是糖尿病肾病形成的重要因素,同时钠钾ATP酶活性增强进一步损伤肾小管功能,一氧化氮升高促使肾小球高灌注、高滤过,也是加速GK大鼠肾病形成的原因.%Objective To establish a CK rat model of type 2 diabetic nephropathv induced by high-calorie and high-protein diet, and to explore its possible mechanism of action. Methods A total of 24 28-week old CK rats were randomly divided into normal group and model group, 12 in each group. The normal rats were given normal diet while the model rats were fed a high-calorie and high-protein diet for 8 weeks. 24 h-U-ALB, 24 h-U-TP, Ucr, U-ALB/Ucr were determined at week 0, 4, and 8. FBG, Scr, BUN, TC, TG, NO were measured at week 4 and 8. The rats were sacrificed 8 weeks later, and the two kidneys of each rat were taken and weighed to calculate the kidney hypertrophy index. The renal pathological changes were examined and the Na+ K+ -ATPase activity in renal tissue was detected. Results The 24 h-U-ALB, 24 h-U-TP, U-ALB/Ucr, FBG, TC, TG, NO, kidney hypertrophy index and Na+ K+-ATPase activity were significantly increased in the model group rats. They showed an increased glomerular volume of the kidney, mesangial matrix hyperplasia and thickening of the glomerular basement membrane. Conclusions A GK rat model of type 2 diabetic nephropathy is successfully established by a high-calorie and high-protein diet. The rise in blood glucose and lipid levels contribute to the development of diabetic nephropathy. Besides, increased activity of Na + K + -ATPase further damages the function of renal tubules. The increased NO leads to glomerular hyperperfusion and hyperfiltration. These factors also accelerate the formation of nephropathy in GK rats.
展开▼
