Yasuda H, Harano Y, Kosugi K, Nakano T, Suzuki M, Tsuruoka Y, Taniguchi Y, Nishimori T, Kikkawa R, Shigeta Y
Diabetes. 1984 May;33(5):415-20. doi: 10.2337/diab.33.5.415.
A chronic diabetic state was produced in Macaca fuscatus , and these diabetic monkeys were kept without insulin treatment for up to 25 mo. The metabolic derangements were characterized by hyperglycemia, insulinopenia, hyperglucagonemia, ketonemia, and hyperlipidemia. Significant thickening of the capillary basement membrane of the gastrocnemius muscle was observed in the chronically diabetic monkeys, and became obvious in the course of diabetic state; 732 +/- 35 A in controls, 750 +/- 58 A in diabetic monkeys with duration of 4 mo, and 1165 +/- 112 A in those with duration of more than 11 mo. In addition to duration of the diabetic state, severity of hyperglycemia is also thought to play an important role in the capillary basement membrane thickening judging from the fact that diabetic monkeys with constant hyperglycemia showed a greater membrane thickening. Ultrastructural alterations, such as significant thickening of glomerular basement membrane and increase of mesangial matrix, were observed in kidney as well. These results indicate that diabetic microangiopathy has been produced by metabolic derangements characterized by chronic hyperglycemia, insulinopenia, and hyperlipidemia.
在食蟹猴中制造出慢性糖尿病状态，这些糖尿病猴在不进行胰岛素治疗的情况下饲养长达25个月。代谢紊乱的特征为高血糖、胰岛素缺乏、高胰高血糖素血症、酮血症和高脂血症。在慢性糖尿病猴中观察到腓肠肌毛细血管基底膜显著增厚，并且在糖尿病状态过程中变得明显；对照组为732±35埃，病程4个月的糖尿病猴为750±58埃，病程超过11个月的糖尿病猴为1165±112埃。从持续高血糖的糖尿病猴显示出更大的基底膜增厚这一事实判断，除了糖尿病状态的持续时间外，高血糖的严重程度也被认为在毛细血管基底膜增厚中起重要作用。在肾脏中也观察到超微结构改变，如肾小球基底膜显著增厚和系膜基质增加。这些结果表明，糖尿病微血管病变是由以慢性高血糖、胰岛素缺乏和高脂血症为特征的代谢紊乱所引起的。
