The physical exercise is a potential strategy to control age-related metabolic disorders, such as insulin resistance, impaired glucose homeostasis, and type 2 diabetes. Rho-kinase (ROCK) increases skeletal muscle glucose uptake through Insulin Receptor Substrate 1 (IRS1) phosphorylation. Here, we investigated the role of physical exercise in ROCK pathway in the skeletal muscle of Fischer middle-aged rats. Firstly, we observed the ROCK distribution in different skeletal muscle fiber types. ROCK signaling pathway (ROCK1 and ROCK2) and activity (pMYPT1) were higher in the soleus, which was associated with increased insulin signaling pathway (pIR, pIRS1, pPDK, pGSK3β). Middle-aged rats submitted to physical exercise, showed the upregulation of ROCK2 content and normalized RhoA (ROCK activator enzyme) levels in soleus muscle compared with middle-aged sedentary rats. These molecular changes in middle-aged exercised rats were accompanied by higher insulin signaling (pIRS1, pGSK3β, pAS160, GLUT4) in the soleus muscle. Reinforcing these findings, when pharmacological inhibition of ROCK activity was performed (using Y-27632), the insulin signaling pathway and glucose metabolism-related genes (Tpi, Pgk1, Pgam2, Eno3) were decreased in the soleus muscle of exercised rats. In summary, ROCK signaling seems to contribute with whole-body glucose homeostasis (∼50 %) through its higher upregulation in the soleus muscle in middle-aged exercised rats.

中文翻译：

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体育锻炼可增加中年大鼠骨骼肌的岩石活性。

体育锻炼是控制与年龄有关的新陈代谢疾病的潜在策略，例如胰岛素抵抗，葡萄糖稳态失衡和2型糖尿病。Rho激酶（ROCK）通过胰岛素受体底物1（IRS1）磷酸化增加骨骼肌葡萄糖摄取。在这里，我们研究了体育锻炼在Fischer中年大鼠骨骼肌ROCK途径中的作用。首先，我们观察了ROCK在不同骨骼肌纤维类型中的分布。比目鱼的ROCK信号通路（ROCK1和ROCK2）和活性（pMYPT1）较高，这与胰岛素信号通路（pIR，pIRS1，pPDK，pGSK3β）增加有关。中年大鼠进行体育锻炼，结果显示，与中年久坐的大鼠相比，比目鱼肌中ROCK2含量和RhoA（ROCK激活酶）水平正常化。这些在中年运动大鼠中的分子变化伴随着比目鱼肌中较高的胰岛素信号传导（pIRS1，pGSK3β，pAS160，GLUT4）。加强这些发现，当进行ROCK活性的药理抑制时（使用Y-27632），运动大鼠的比目鱼肌中胰岛素信号通路和葡萄糖代谢相关基因（Tpi，Pgk1，Pgam2，Eno3）降低。总之，ROCK信号似乎通过中年运动大鼠比目鱼肌中的更高的上调而促进全身葡萄糖稳态（〜50％）。比目鱼肌中的pGSK3β，pAS160，GLUT4）。加强这些发现，当进行ROCK活性的药理抑制时（使用Y-27632），运动大鼠的比目鱼肌中胰岛素信号通路和葡萄糖代谢相关基因（Tpi，Pgk1，Pgam2，Eno3）降低。总之，ROCK信号似乎通过中年运动大鼠比目鱼肌中的更高的上调而促进全身葡萄糖稳态（〜50％）。比目鱼肌中的pGSK3β，pAS160，GLUT4）。加强这些发现，当进行ROCK活性的药理抑制时（使用Y-27632），运动大鼠的比目鱼肌中胰岛素信号通路和葡萄糖代谢相关基因（Tpi，Pgk1，Pgam2，Eno3）降低。总之，ROCK信号似乎通过中年运动大鼠比目鱼肌中的更高的上调而促进全身葡萄糖稳态（〜50％）。