Mokhtar N, Lavoie J P, Rousseau-Migneron S, Nadeau A
Diabetes Research Unit, Laval University Medical Center, Ste-Foy, Quebec, Canada.
Diabetes. 1993 May;42(5):682-7. doi: 10.2337/diab.42.5.682.
This study examined the impact of physical training on cardiac mitochondrial respiration of rats with chronic diabetes mellitus. Diabetes was induced by an intravenous injection of STZ (50 mg/kg) and only rats with a blood glucose level between 14 and 22 mM 1 wk later were kept in the protocol. Exercise training was conducted on a treadmill with a progressive 10-wk program. Animals were killed at the end of the training program, and mitochondria were isolated from ventricular tissue by differential centrifugation. Both state 3 respiration and oxidative phosphorylation rates were depressed significantly in the mitochondria of diabetic rats. These alterations were reversed completely to normal by physical training, without any significant changes in plasma glucose or insulin levels. The activity of ANT was not affected by diabetes or training. These results indicate that the depressed OPR present in isolated heart mitochondria from chronically diabetic rats is reversed to normal by physical training, apparently by mechanisms independent of blood glucose control. This correction in mitochondrial energy production may explain the improvement in cardiac function previously reported in trained diabetic rats.
本研究考察了体育锻炼对慢性糖尿病大鼠心脏线粒体呼吸的影响。通过静脉注射链脲佐菌素（STZ，50 mg/kg）诱导糖尿病，仅将1周后血糖水平在14至22 mM之间的大鼠纳入实验方案。采用渐进式10周方案在跑步机上进行运动训练。在训练方案结束时处死动物，通过差速离心从心室组织中分离出线粒体。糖尿病大鼠线粒体的状态3呼吸和氧化磷酸化速率均显著降低。通过体育锻炼，这些改变完全恢复正常，而血浆葡萄糖或胰岛素水平无任何显著变化。腺苷酸转运体（ANT）的活性不受糖尿病或训练的影响。这些结果表明，长期糖尿病大鼠分离的心脏线粒体中存在的氧化磷酸化速率降低通过体育锻炼恢复正常，显然是通过独立于血糖控制的机制。线粒体能量产生的这种纠正可能解释了先前报道的训练糖尿病大鼠心脏功能的改善。
