Pattamaprapanont Pattarawan, Muanprasat Chatchai, Soodvilai Sunhapas, Srimaroeng Chutima, Chatsudthipong Varanuj
Department of Physiology, Faculty of Science, Mahidol University, Rama 6 Rd, Rajathevi, Bangkok, 10400, Thailand.
Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.
Rev Diabet Stud. 2016 Summer-Fall;13(2-3):197-206. doi: 10.1900/RDS.2016.13.197. Epub 2016 Aug 10.
Diabetes and exercise training have been shown to involve interleukin 6 (IL-6) signaling in muscle. However, the relationship between the actions of these two stimuli on muscle IL-6 and their downstream components is still unknown. Thus, the effect of endurance training on the key components of muscle IL-6 signaling transduction was investigated in a rat model of type 2 diabetes.
Diabetes was induced by streptozotocin (STZ) in male Wistar rats fed a high-fat diet, with normal rats acting as controls. The animals were left to conduct their normal activities or assigned to endurance training in a treadmill. At the end of 8 weeks, blood biochemical profiles, exercise performance, muscle oxidative capacity, glucose transporter 4 (GLUT4) protein distribution, and expressions of IL-6 and its downstream proteins were determined.
Blood biochemical profiles of the diabetic rats were altered compared to normal rats, whereas endurance training improved blood chemistry and exercise performance. It also increased muscle oxidative capacity, and promoted GLUT4 subcellular localization to the membrane in muscles. Furthermore, protein expression of IL-6 receptor (IL-6Rα) was increased in both normal and diabetic rats after endurance training, but no significant changes in IL-6, phosphorylated signal transducer and activator of transcription 3 (p-STAT3), or suppressor of cytokine signaling 3 (SOC3) were observed in muscles of normal and diabetic rats.
IL-6 signaling pathway mediating muscle response to endurance training was conserved in type 2 diabetes. There was no link between training-induced IL-6 downstream targets in skeletal muscles and IL-6-induced type 2 diabetes.
糖尿病和运动训练已被证明与肌肉中的白细胞介素6（IL-6）信号传导有关。然而，这两种刺激对肌肉IL-6及其下游成分的作用之间的关系仍然未知。因此，在2型糖尿病大鼠模型中研究了耐力训练对肌肉IL-6信号转导关键成分的影响。
用链脲佐菌素（STZ）诱导雄性Wistar大鼠患糖尿病，这些大鼠喂食高脂饮食，正常大鼠作为对照。让动物进行正常活动或分配到跑步机上进行耐力训练。在8周结束时，测定血液生化指标、运动能力、肌肉氧化能力、葡萄糖转运蛋白4（GLUT4）蛋白分布以及IL-6及其下游蛋白的表达。
与正常大鼠相比，糖尿病大鼠的血液生化指标发生了改变，而耐力训练改善了血液生化指标和运动能力。它还增加了肌肉氧化能力，并促进了GLUT4在肌肉中的亚细胞定位到细胞膜。此外，耐力训练后正常大鼠和糖尿病大鼠的IL-6受体（IL-6Rα）蛋白表达均增加，但在正常大鼠和糖尿病大鼠的肌肉中未观察到IL-6、磷酸化信号转导和转录激活因子3（p-STAT3）或细胞因子信号抑制因子3（SOC3）有显著变化。
介导肌肉对耐力训练反应的IL-6信号通路在2型糖尿病中是保守的。骨骼肌中训练诱导的IL-6下游靶点与IL-6诱导的2型糖尿病之间没有联系。
