The effect of endurance training on levels of LINC complex proteins in skeletal muscle fibers of STZ-induced diabetic rats

耐力训练对STZ诱发的糖尿病大鼠骨骼肌纤维LINC复合蛋白水平的影响

阅读:5
作者:Mehdi Bostani, Masoud Rahmati, Seyyed Ali Mard

Abstract

The changes of the linker of nucleoskeleton and cytoskeleton (LINC) complex have been studied in many muscular abnormality conditions; however, the effects of diabetes and physical activities on it have still remained to be defined. Therefore, the purpose of the this study was to evaluate the impacts of a six-week endurance training on the levels of SUN1 and Nesprin-1 proteins in Soleus and EDL muscles from diabetic wistar rats. A total number of 48 male Wistar rats (10 weeks, 200-250 gr) were randomly divided into healthy control (HC, N = 12), healthy trained (HT, N = 12), diabetic control (DC, N = 12), and diabetic trained (DT, N = 12) groups. Diabetes was also induced by a single intraperitoneally injection of streptozocin (45 mg/kg). The training groups ran a treadmill for five consecutive days within six weeks. The levels of the SUN1 and the Nesprin-1 proteins were further determined via ELISA method. The induction of diabetes had significantly decreased the levels of Nesprin-1 protein in the soleus and EDL muscles but it had no effects on the SUN1 in these muscles. As well, the findings revealed that six weeks of endurance training had significantly increased the levels of Nesprin-1 in DT and HT groups in the soleus as well as the EDL muscles; however, it had no impacts on the SUN1 in these muscles. The muscle fiber cross-sectional area (CSA) and myonuclei also decreased in diabetic control rats in both studied muscles. The training further augmented these parameters in both studied muscles in HT and DT groups. The present study provides new evidence that diabetes changes Nesprin-1 protein levels in skeletal muscle and endurance exercise training can modify it.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。