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作 者:覃乔静[1] 邓华聪[1] 曹文富[1] 兰丽珍[1] 刘东方[1]
机构地区:[1]重庆医科大学附属第一医院内分泌科,400016
出 处:《临床内科杂志》2004年第3期202-204,共3页Journal of Clinical Internal Medicine
摘 要:目的 观察糖脂代谢紊乱对糖尿病大鼠肾小球滤过屏障外层足细胞的影响 ,以探讨糖尿病肾病的发病机制。方法 采用链脲佐菌素诱导糖尿病大鼠模型 ,喂养 5周后 ,测定血糖、糖化血红蛋白、甘油三酯、总胆固醇、血肌酐、尿素氮和尿白蛋白排泄率 ,应用免疫组化检测肾小球足细胞损伤标志蛋白 -desmin的表达 ,同时利用透射电子显微镜观察肾小球足细胞超微结构。结果 糖尿病大鼠血糖、糖化血红蛋白、总胆固醇、血肌酐、尿素氮、尿白蛋白排泄率水平明显升高 (P <0 .0 5 ) ,肾小球内desmin蛋白表达上调 ,足细胞部分足突融合 ;同时 ,两组间血甘油三酯水平无显著性差异 (P >0 .0 5 )。结论 糖脂代谢紊乱可导致糖尿病大鼠肾小球滤过屏障外层足细胞明显损害 ,尿白蛋白排泄率增加 ,这可能是糖尿病肾脏损害。Objective To investigate the influence of glucose and lipid metabolic disorders on podocyte,the last barrier of glomerular filtration,to research the pathogenesis of diabetic nephropathy.Methods Diabetic rats were induced by streptozotocin(STZ).The levels of glucose(BG),HbA1c,triglyceride (TG),total cholesterol(TC),creatinine(Cr),urea nitrogen(Bun) in blood and urinary albumin excretion rate(UAER) were measured after 5 weeks.Immunohistochemistry was used to detect the expression of desmin,a marker of podocyte injury.In addition, the podocyte ultrastructure was observed by transmission electronic microscopy.Results Compared with normal group,the levels of BG,HbA1c,TC,Cr,Bun in blood and UAER increased markedly accompanied with increased expression of glomerular desmin in diabetic group(P<0.05).There was no significant change among groups on the levels of TG in blood(P>0.05).Foot process effacement in podocytes could be found in diabetic group.Conclusion The glucose and lipid metabolic disorders could markedly injure podocyte,the last barrier of glomerular filtration,to increase UAER indiabetic rats.It may be the pathogenesis of renal injury and proteinuria in diabetes.
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