高热量高蛋白饮食诱导GK大鼠糖尿病肾病模型的建立
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徐孝平(1978-),男,实验师,研究方向:实验动物与比较医学。E-mail: xxp0001@126.com。

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浙江省科技厅实验动物计划项目(编号:2009F80021)。


Establishment of a GK Rat Model of Diabetic Nephropathy Induced by High-Calorie and High-Protein Diet
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    摘要:

    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、24 h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。

    Abstract:

    ObjectiveTo establish a GK rat model of type 2 diabetic nephropathy induced by high-calorie and high-protein diet, and to explore its possible mechanism of action. MethodsA total of 24 28-week old GK 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. ResultsThe 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. ConclusionsA 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. 

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徐孝平,寿旗扬,陈方明,周卫民,蔡月琴,陈民利.高热量高蛋白饮食诱导GK大鼠糖尿病肾病模型的建立[J].中国比较医学杂志,2012,(4):53~57.

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