Na Ha-Na, Hong Young-Mi, Ye Michael B, Park Sooho, Kim In-Beom, Nam Jae-Hwan
Department of Biotechnology, The Catholic University of Korea, Bucheon, Republic of Korea.
Department of Pediatrics, Ewha Womans University Medical School, Seoul, Republic of Korea.
PLoS One. 2014 Dec 5;9(12):e114534. doi: 10.1371/journal.pone.0114534. eCollection 2014.
Human adenovirus type 36 (Ad36) as an obesity agent induces adiposity by increasing glucose uptake and promoting chronic inflammation in fat tissues; in contrast, exercise reduces total body fat and inflammation. Our objective was to determine the association between Ad36 and the effects of exercise on inflammation and glycemic control. In the human trials (n = 54), Korean children (aged 12-14 years) exercised for 60 min on three occasions each week for 2 months. We compared the body mass index (BMI) Z-scores before and after exercise. C57BL/6 mice were infected with Ad36 and Ad2 as a control, and these mice exercised for 12 weeks postinfection. After the exercise period, we determined the serum parameters and assessed the presence of inflammation and the mitochondrial function in the organs. Ad36-seropositive children who were subjected to a supervised exercise regimen had high BMI Z-scores whereas Ad36-seronegative children had lower scores. Similarly, Ad36-infected mice were resistant to weight loss and exhibited chronic inflammation of their adipose tissues despite frequent exercise. However, Ad36 combined with exercise reduced the levels of serum glucose, nonesterified fatty acids, total cholesterol, and insulin in virus-infected mice. Interestingly, virus infection increased the mitochondrial function in the liver, as demonstrated by the numbers of mitochondria, cytochrome c oxidase activity, and transcription of key mitochondrial genes. Therefore Ad36 counteracts the weight-loss effect of exercise and maintains the chronic inflammatory state, but glycemic control is improved by exercise synergistically because of increased mitochondrial activity in the liver.
36型人腺病毒（Ad36）作为一种致肥胖因子，通过增加葡萄糖摄取和促进脂肪组织中的慢性炎症来诱导肥胖；相比之下，运动可减少全身脂肪和炎症。我们的目的是确定Ad36与运动对炎症和血糖控制影响之间的关联。在人体试验（n = 54）中，韩国儿童（12 - 14岁）每周三次、每次锻炼60分钟，持续2个月。我们比较了运动前后的体重指数（BMI）Z评分。将C57BL/6小鼠感染Ad36和作为对照的Ad2，并在感染后让这些小鼠运动12周。运动期结束后，我们测定了血清参数，并评估了器官中炎症的存在情况和线粒体功能。接受监督运动方案的Ad36血清阳性儿童的BMI Z评分较高，而Ad36血清阴性儿童的评分较低。同样，尽管频繁运动，Ad36感染的小鼠对体重减轻具有抗性，并表现出脂肪组织的慢性炎症。然而，Ad36与运动相结合可降低病毒感染小鼠的血清葡萄糖、非酯化脂肪酸、总胆固醇和胰岛素水平。有趣的是，病毒感染增加了肝脏中的线粒体功能，这通过线粒体数量、细胞色素c氧化酶活性和关键线粒体基因的转录得以证明。因此，Ad36抵消了运动的减肥效果并维持慢性炎症状态，但由于肝脏中线粒体活性增加，运动协同改善了血糖控制。
