Pierce G N, Dhalla N S
Can J Cardiol. 1985 Jan;1(1):48-54.
Diabetes was introduced in rats by an intravenous injection of streptozotocin (65 mg/kg). Animals were sacrificed 8 weeks later and mitochondria were isolated from the ventricular tissue by differential centrifugation. The state 3 respiration, oxidative phosphorylation rate and Mg2+-dependent ATPase activities were depressed in mitochondria from diabetic hearts. These changes were partially reversible upon 2 weeks of insulin and fully reversible after 4 weeks of insulin therapy. Mitochondrial calcium uptake but not calcium binding, was decreased in diabetes and this change was fully reversible by 2 weeks of insulin administration. The observed alterations in mitochondrial function could not be explained on the basis of any changes in mitochondrial lipid and protein composition or subcellular contamination. These results indicate the presence of a generalized depression in mitochondrial function in chronic diabetes and such a defect is suggested to contribute in the development of cardiomyopathy at late stages of diabetes.
通过静脉注射链脲佐菌素（65毫克/千克）在大鼠中诱发糖尿病。8周后处死动物，通过差速离心从心室组织中分离出线粒体。糖尿病心脏的线粒体中状态3呼吸、氧化磷酸化率和镁离子依赖性ATP酶活性均降低。这些变化在胰岛素治疗2周后部分可逆，4周后完全可逆。糖尿病时线粒体钙摄取减少，但钙结合无变化，胰岛素给药2周后这种变化完全可逆。观察到的线粒体功能改变不能用线粒体脂质和蛋白质组成或亚细胞污染的任何变化来解释。这些结果表明慢性糖尿病中线粒体功能普遍存在抑制，这种缺陷被认为在糖尿病晚期心肌病的发展中起作用。
