高果糖饮食对大鼠肾脏的毒性作用

 [摘要] 目的　观察高果糖饮食诱导的高甘油三酯血症对大鼠肾组织病理形态的影响，探讨脂质肾毒性的作用机制。方法 将32只大鼠分为正常对照组(N组,n=16)及高果糖组(F组,n=16)，8及16周时分批处死，检测各组大鼠的肾功能、空腹血糖、血脂及24h尿微量白蛋白；检测大鼠肾皮质甘油三酯含量；采用免疫组化分析IV型胶原及α-平滑肌动蛋白表达和定位，并观察肾脏病理变化。电镜观察肾脏基底膜变化。结果　8周和16周时，高果糖组血中甘油三酯分别达(1.65+0.86)mmol/L、（2.13+0.87）mmol/L，极低密度脂蛋白分别达(0.75+0.39)mmol/L、(0.97+0.40)mmol/L，肾组织中甘油三酯分别达(7.21+2.20)mg/g、(7.92+3.05)mg/g，24h尿微量白蛋白分别达(63.00+12.00)μg、(150.00+48.00) μg，较对照组明显升高（P<0.05）；肾脏病理改变加重，基底膜增厚，肾组织IV型胶原α-SMA表达明显增加（P<0.05）。结论　高果糖饮食可诱导大鼠高甘油三酯血症，并使肾组织油三酯水平增加导致肾脏损伤。

Effect of high fructose-induced hypertriglyceridmia on kidney of rats

[Abstract] Objective To investigate the effect of high fructose-induced hypertriglyceridmia on kidney of healthy Wistar rats. Methods Thirty-two healthy male Wistar rats were randomly divided into two groups (n =16): normal control group and high fructose group. Rats were sacrificed by the end of 8 and 16 weeks. BUN, Scr, fast glucose ,lipid concentration, urinary microalbumin were observed. Triglyceride of renal cortices were detected. The pathological changes were examined by PAS staining. IV-type collage and α-SMA protein were examined by immunohistochemistry staining. The electron microscope sections were made to measure GBM width Results By the end of 8 and 16 weeks, compared with the control group, high fructose group showed elevated triglyceride (1.65+0.86)mmol/L、（2.13+0.87）mmol/L(both P<0.05 ), and very low density lipoprotein chloesterol(0.75+0.39)mmol/L、(0.97+0.40)mmol/L(both P<0.05 ) in blood. Renal cortices were both significantly increased(7.21+2.20)mg/g、(7.92+3.05)mg/g (both P<0.05). The urinary microalbumin significantly increased too(63.00+12.00)μg、(150.00+48.00) μg (both P<0.05). The pathological changes were serious in the high fructose group. The expression of IV-type collagen and α-SMA protein were up-regulated. Electron microscope revealed GBM obviously thickened in high fructose group. Conclusion High fructose-induced hypertriglyceridmia may cause lipid nephrotoxicity in Wistar rats.