链脲佐菌素诱导的糖尿病大鼠肾小球阴离子位点丧失与蛋白尿的发生
Loss of glomerular anionic sites and the development of albuminuria in rats with streptozotocin-induced diabetes.
作者信息
Moriya T, Nakazawa K, Itoh N, Shigematsu H, Okada N, Aizawa T, Yamada T, Yajima Y
机构信息
Department of Internal Medicine, Kitasato University School of Medicine, Sagamihara, Japan.
出版信息
Nephron. 1993;65(3):444-8. doi: 10.1159/000187527.
Examination was made of changes in the anionic sites of the glomerular basement membrane (GBM) in rats with streptozotocin (STZ)-induced diabetes by the immersion method of polyethyleneimine (PEI). PEI particles in GBM of diabetic rats significantly decreased from the 1st through the 8th week. Urinary albumin excretion in diabetic rats significantly increased at the 2nd but not earlier week. Insulin treatment effectively prevented decrease in PEI particles in STZ-injected rats. In rats with STZ-induced diabetes, initial renal alteration was disturbance of the charge barrier, followed by the development of albuminuria. Continued deterioration of anionic sites and possibly additional disturbance of size barrier were considered responsible for the development of albuminuria. Insulin treatment appears to prevent the loss of anionic sites of GBM.
采用聚乙烯亚胺（PEI）浸渍法，对链脲佐菌素（STZ）诱导的糖尿病大鼠肾小球基底膜（GBM）阴离子位点的变化进行了研究。糖尿病大鼠GBM中的PEI颗粒在第1周至第8周显著减少。糖尿病大鼠尿白蛋白排泄在第2周而非更早时显著增加。胰岛素治疗有效预防了STZ注射大鼠中PEI颗粒的减少。在STZ诱导的糖尿病大鼠中，最初的肾脏改变是电荷屏障的紊乱，随后出现蛋白尿。阴离子位点的持续恶化以及可能的大小屏障的额外紊乱被认为是蛋白尿发生的原因。胰岛素治疗似乎可预防GBM阴离子位点的丢失。
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