RETARDATION BY AMINOGUANIDINE OF DEVELOPMENT OF ALBUMINURIA, MESANGIAL EXPANSION, AND TISSUE FLUORESCENCE IN STREPTOZOCIN-INDUCED DIABETIC RAT
RETARDATION BY AMINOGUANIDINE OF DEVELOPMENT OF ALBUMINURIA, MESANGIAL EXPANSION, AND TISSUE FLUORESCENCE IN STREPTOZOCIN-INDUCED DIABETIC RAT
复制标题
DOI：
10.2337/diabetes.40.10.1328
复制
发表时间：
1991-10-01
期刊：
影响因子：
7.7
通讯作者：
JERUMS, G
中科院分区：
文献类型：
--
作者：
SOULISLIPAROTA, T;COOPER, M;JERUMS, G
这项研究评估了 32 周内肾脏中晚期糖基化终产物 (AGE) 相关荧光的发展与实验性糖尿病肾病之间的关系。 对对照、未经治疗的糖尿病大鼠和经氨基胍治疗的糖尿病大鼠进行为期 32 周的随访，每周测量 8 次尿白蛋白排泄量。 32周后，评估主动脉和肾脏（全肾、离体肾小球和肾小管）中胶原蛋白相关的荧光以及肾小球超微结构。 糖尿病与主动脉和肾脏中胶原蛋白相关荧光的显着增加有关。 氨基胍可防止主动脉、离体肾小球和肾小管中胶原蛋白相关荧光的增加，但不能防止整个肾脏中胶原蛋白相关荧光的增加。 糖尿病与白蛋白尿、系膜体积分数和肾小球基底膜（GBM）厚度增加有关。 氨基胍可减弱糖尿病大鼠白蛋白尿的增加并防止系膜扩张，而不影响糖尿病大鼠的 GBM 厚度。 氨基胍治疗引起的胶原蛋白相关荧光、蛋白尿和系膜扩张的伴随变化与 AGE 可能在糖尿病肾病的发展中发挥作用的假设一致。
This study evaluated the relationship between the development of fluorescence related to advanced glycosylation end products (AGEs) in the kidney and experimental diabetic nephropathy over a 32-wk period. Control, untreated diabetic, and aminoguanidine-treated diabetic rats were followed for 32 wk with eight weekly measurements of urinary albumin excretion. After 32 wk, collagen-related fluorescence in aorta and kidney (whole kidney, isolated glomeruli, and renal tubules) and glomerular ultrastructure were evaluated. Diabetes was associated with a significant increase in collagen-related fluorescence in the aorta and kidney. Aminoguanidine prevented the increases in collagen-related fluorescence in aorta, isolated glomeruli, and renal tubules but not in whole kidney. Diabetes was associated with increased albuminuria, fractional mesangial volume, and glomerular basement membrane (GBM) thickness. Aminoguanidine attenuated the rise in albuminuria and prevented mesangial expansion without influencing GBM thickness in diabetic rats. The concomitant changes in collagen-related fluorescence, albuminuria, and mesangial expansion with aminoguanidine therapy are consistent with the hypothesis that AGEs may play a role in the development of diabetic nephropathy.