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 for checking the BUN, Scr, fast glucose, lipid concentration, urinary microalbumin and triglyceride. The pathological changes were examined by PAS staining. Ⅳ-type collage and α-SMA protein were examined by immunohistochemistry staining. The EM sections were prepared to measure GBM width. Results By the end of 8 and 16 weeks, high fructose group showed elevated triglyceride and very low density lipoprotein chloesterol in blood. Triglyceride of renal cortices were both significantly increased. The urinary microalbumin significantly increased too ( P < 0. 05 ). The pathological changes were evident in the high fructose group. The expression of Ⅳ-type collagen and α-SMA protein were up-regulated, the absorbance ratio of immunohistochemistry stain were 0.427 ±0.017 and 0.240 ± 0. 014, obviously higher than that of control group 0. 325 ±0. 015 and 0. 115 ±0. 012. Electron microscopy revealed GBM obviously thickened in high fructose group. Conclusions High fructose-induced hypertriglyceridmia may cause lipid nephro-toxicity in Wistar rats.%目的 观察高果糖饮食诱导的高三酰甘油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=16)、高果糖组(n=16),8、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;检测大鼠肾皮质三酰甘油含量;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、16周时,高果糖组血中三酰甘油和极低密度脂蛋白,以及肾组织中三酰甘油和24h尿微量白蛋白均较对照组明显升高(P＜0.05);肾脏病理改变加重,基底膜增厚.16周时肾组织Ⅳ型胶原和α-SMA分别为0.427±0.017和0.240±0.014,均显著高于对照组的0.325±0.015和0.115±0.012(P＜0.01).结论 高果糖饮食可诱导大鼠高三酰甘油血症,并使肾组织三酰甘油水平增加导致肾脏损伤.
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