氨基胍可延长氮质血症诱导的糖尿病大鼠的生存期。

Aminoguanidine prolongs survival in azotemic-induced diabetic rats.

作者信息

Friedman E A, Distant D A, Fleishhacker J F, Boyd T A, Cartwright K

机构信息

Department of Medicine, State University of New York, Health Science Center at Brooklyn, 11203-2098, USA.

出版信息

Am J Kidney Dis. 1997 Aug;30(2):253-9. doi: 10.1016/s0272-6386(97)90060-3.

DOI:10.1016/s0272-6386(97)90060-3

PMID:9261037

Abstract

Toxic effects of hyperglycemia-induced advanced glycosylated end products (AGEs) may explain some vasculopathic complications of diabetes. Aminoguanidine, a known inhibitor of AGE formation, was administered by gavage to Sprague-Dawley streptozotocin-induced diabetic rats made azotemic by surgical reduction of renal mass. All rats became hyperglycemic. Renal ablation caused renal insufficiency, as evidenced by markedly reduced endogenous creatinine clearances at days 7 and 14. Aminoguanidine-treated rats had significantly (P < 0.04) superior survival to that of untreated azotemic diabetic rats. We infer from the extended life in a rat model of uremia in diabetic nephropathy that aminoguanidine may prove beneficial in human diabetes.

摘要

高血糖诱导的晚期糖基化终产物（AGEs）的毒性作用可能解释了糖尿病的一些血管病变并发症。氨基胍是一种已知的AGE形成抑制剂，通过灌胃给予经链脲佐菌素诱导的Sprague-Dawley糖尿病大鼠，这些大鼠通过手术减少肾质量而产生氮质血症。所有大鼠均出现高血糖。肾切除导致肾功能不全，第7天和第14天内源性肌酐清除率显著降低证明了这一点。氨基胍治疗的大鼠的生存率显著高于未治疗的氮质血症糖尿病大鼠（P < 0.04）。我们从糖尿病肾病尿毒症大鼠模型的延长寿命推断，氨基胍可能对人类糖尿病有益。