el Midaoui A, Tancrède G, Nadeau A
Diabetes Research Unit, Research Center of Laval University Medical Center, Ste-Foy, Quebec, Canada.
Metabolism. 1996 Jul;45(7):810-6. doi: 10.1016/s0026-0495(96)90151-1.
The study was designed to assess the impact of physical training on the oxidative phosphorylation rate (OPR) in mitochondria isolated from two different skeletal muscles of rats with or without chronic diabetes mellitus. Diabetes was induced by an intravenous injection of streptozotocin (50 mg/kg), and only animals with a blood glucose level between 14 and 22 mmol/L 1 week later were kept in the protocol. Exercise training was performed on a treadmill with a progressive 10-week program. Rats were killed by decapitation at the end of the training program, and mitochondria were isolated from the gastrocnemius and the red vastus lateralis muscles. When the data were expressed as per milligrams of protein, OPR was significantly depressed by diabetes mellitus in the mitochondria from each muscle; a similar negative impact also appeared to be produced by physical training in mitochondria isolated from the red vastus lateralis muscle. However, due to changes in mitochondrial protein yield between groups, the capacity to oxidize pyruvate and malate was also calculated per gram of muscle. Adenosine triphosphate (ATP) production rate appeared to be unaffected by diabetes but significantly increased by training in both muscles of diabetic and nondiabetic rats. This effect of training was not associated with any improvement in plasma glucose or insulin levels in diabetic animals. However, the large increase in plasma levels of beta-hydroxybutyric acid in sedentary diabetic rats was partly reversed by training (1,079 +/- 472 v 3,424 +/- 618 micromol, P < .001). These results suggest that the training-induced increase in the capacity of skeletal muscles to oxidize substrates and generate energy may also contribute to reduce the elevated plasma beta-hydroxybutyric acid levels observed in a state of insulin deficiency. This may have clinical relevance, since ketoacidosis remains a life-threatening event in insulin-dependent diabetic subjects.
该研究旨在评估体育训练对从患有或未患慢性糖尿病的大鼠的两种不同骨骼肌中分离出的线粒体氧化磷酸化率（OPR）的影响。通过静脉注射链脲佐菌素（50mg/kg）诱导糖尿病，仅将1周后血糖水平在14至22mmol/L之间的动物纳入实验方案。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，通过断头处死大鼠，并从腓肠肌和股外侧肌分离出线粒体。当数据以每毫克蛋白质表示时，糖尿病显著降低了每块肌肉线粒体中的OPR；体育训练对从股外侧肌分离出的线粒体似乎也产生了类似的负面影响。然而，由于各组线粒体蛋白质产量的变化，还计算了每克肌肉氧化丙酮酸和苹果酸的能力。三磷酸腺苷（ATP）产生率似乎不受糖尿病影响，但在糖尿病和非糖尿病大鼠的两块肌肉中，训练均使其显著增加。训练的这种作用与糖尿病动物的血糖或胰岛素水平的任何改善均无关。然而，久坐的糖尿病大鼠血浆β-羟基丁酸水平的大幅升高通过训练得到了部分逆转（1,079±472对3,424±618μmol，P<.001）。这些结果表明，训练诱导的骨骼肌氧化底物和产生能量能力的增加也可能有助于降低在胰岛素缺乏状态下观察到的血浆β-羟基丁酸水平升高。这可能具有临床相关性，因为酮症酸中毒在胰岛素依赖型糖尿病患者中仍然是危及生命的事件。
