Combination of exercise training and diet restriction normalizes limited exercise capacity and impaired skeletal muscle function in diet-induced diabetic mice.
Combination of exercise training and diet restriction normalizes limited exercise capacity and impaired skeletal muscle function in diet-induced diabetic mice.
复制标题
DOI：
10.1210/en.2013-1382
复制
发表时间：
2014
期刊：
影响因子：
4.8
通讯作者：
T. Suga;S. Kinugawa;S. Takada;Tomoyasu Kadoguchi;A. Fukushima;Tsuneaki Homma;Yoshihiro Masaki;T. Furihata;Masashige Takahashi;M. A. Sobirin;Taisuke Ono;K. Hirabayashi;T. Yokota;S. Tanaka;K. Okita;H. Tsutsui
中科院分区：
文献类型：
--
作者：
T. Suga;S. Kinugawa;S. Takada;Tomoyasu Kadoguchi;A. Fukushima;Tsuneaki Homma;Yoshihiro Masaki;T. Furihata;Masashige Takahashi;M. A. Sobirin;Taisuke Ono;K. Hirabayashi;T. Yokota;S. Tanaka;K. Okita;H. Tsutsui
运动训练（EX）和饮食限制（DR）是有效控制糖尿病肥胖和胰岛素抵抗的关键。然而，这些干预措施是否能改善糖尿病患者有限的运动能力和受损的骨骼肌功能仍有待研究。因此，我们研究了EX和/或DR对饮食诱导的糖尿病小鼠运动能力和骨骼肌功能的影响。将喂食高脂饮食（HFD）8周的雄性C57 BL/6 J小鼠随机分配另外4周至4组：对照组、EX组、DR组和EX+ DR组。还研究了喂食正常饮食的瘦型组。由HFD诱导的肥胖和胰岛素抵抗被EX或DR显著但部分地改善，并且被EX+ DR完全逆转。尽管与正常饮食相比，HFD的运动能力显著降低，但EX和DR部分改善，EX+ DR完全逆转。由HFD引起的骨骼肌中受损的线粒体功能和增强的氧化应激仅通过EX+恢复正常。虽然肥胖和胰岛素抵抗完全逆转DR与胰岛素增敏药物或长期干预，运动能力和骨骼肌功能不能正常化。因此，改善受损的骨骼肌功能，而不是肥胖和胰岛素抵抗，可能是糖尿病患者有限运动能力正常化的重要治疗目标。总之，运动和饮食的综合生活方式疗法可以使糖尿病患者有限的运动能力和受损的肌肉功能恢复正常。
Exercise training (EX) and diet restriction (DR) are essential for effective management of obesity and insulin resistance in diabetes mellitus. However, whether these interventions ameliorate the limited exercise capacity and impaired skeletal muscle function in diabetes patients remains unexplored. Therefore, we investigated the effects of EX and/or DR on exercise capacity and skeletal muscle function in diet-induced diabetic mice. Male C57BL/6J mice that were fed a high-fat diet (HFD) for 8 weeks were randomly assigned for an additional 4 weeks to 4 groups: control, EX, DR, and EX+DR. A lean group fed with a normal diet was also studied. Obesity and insulin resistance induced by a HFD were significantly but partially improved by EX or DR and completely reversed by EX+DR. Although exercise capacity decreased significantly with HFD compared with normal diet, it partially improved with EX and DR and completely reversed with EX+DR. In parallel, the impaired mitochondrial function and enhanced oxidative stress in the skeletal muscle caused by the HFD were normalized only by EX+DR. Although obesity and insulin resistance were completely reversed by DR with an insulin-sensitizing drug or a long-term intervention, the exercise capacity and skeletal muscle function could not be normalized. Therefore, improvement in impaired skeletal muscle function, rather than obesity and insulin resistance, may be an important therapeutic target for normalization of the limited exercise capacity in diabetes. In conclusion, a comprehensive lifestyle therapy of exercise and diet normalizes the limited exercise capacity and impaired muscle function in diabetes mellitus.