Volume 26, Issue 4 (10-2024)
yafte 2024, 26(4): 79-91 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Garavandpour F, Valipour Dehnou V, Eslami R. Studying GLUT5 protein levels in response to diabetes and endurance training in the EDL muscle of mice. yafte 2024; 26 (4) :79-91
URL: http://yafte.lums.ac.ir/article-1-3764-en.html
URL: http://yafte.lums.ac.ir/article-1-3764-en.html
Department of Sports Sciences, Faculty of Literature and Human Sciences, Lorestan University, Khorramabad, Iran & Department of Sports Sciences, Faculty of Literature and Human Sciences, Lorestan University, Khorramabad, Iran
Abstract: (1859 Views)
Background: Type 2 diabetes is the most common chronic disease characterized by insulin resistance and disruption of glucose membrane transport mechanisms. It has been shown that GLUT5 and AS160 proteins play a role in this mechanism. Therefore, the aim of the present study was to investigate the effect of endurance training on the levels of GLUT5, AS160, and insulin resistance in the extensor digitorum longus (EDL) muscle of type 2 diabetic rats.
Materials and Methods: A total of 30 adult male laboratory mice were randomly divided into 3 groups: control (C), diabetes (D), and diabetes training (DT). Diabetes was induced by streptozotocin (35 ml/kg) injection and a high-fat diet. Endurance training consisted of five sessions of treadmill running each week for 8 weeks. EDL muscle extraction was done 48 hours after the last training session. The enzyme-linked immunosorbent assay method was used to measure proteins. To analyze the data, a one-way analysis of variance was used at a significance level of 0.05.
Results: There was no significant difference between GLUT5 levels in all groups (P=0.94). However, AS160 levels were higher in the C group than in the other two groups (P=0.001). Moreover, AS160 levels were significantly higher in the DT group than in the D group (P=0.001). There was no significant correlation between GLUT5 and AS160 (r=0.02, P=0.94).
Conclusion: Endurance training, by compensating the destructive mechanisms of diabetes, reduces hyperglycemia and overexpression of AS160 protein levels in EDL muscle; however, it does not affect GLUT5 protein levels. Therefore, it seems that endurance training plays a role in modulating the damaging effects of diabetes in skeletal muscles through mechanisms other than increasing GLUT5, such as changes in AS160.
Materials and Methods: A total of 30 adult male laboratory mice were randomly divided into 3 groups: control (C), diabetes (D), and diabetes training (DT). Diabetes was induced by streptozotocin (35 ml/kg) injection and a high-fat diet. Endurance training consisted of five sessions of treadmill running each week for 8 weeks. EDL muscle extraction was done 48 hours after the last training session. The enzyme-linked immunosorbent assay method was used to measure proteins. To analyze the data, a one-way analysis of variance was used at a significance level of 0.05.
Results: There was no significant difference between GLUT5 levels in all groups (P=0.94). However, AS160 levels were higher in the C group than in the other two groups (P=0.001). Moreover, AS160 levels were significantly higher in the DT group than in the D group (P=0.001). There was no significant correlation between GLUT5 and AS160 (r=0.02, P=0.94).
Conclusion: Endurance training, by compensating the destructive mechanisms of diabetes, reduces hyperglycemia and overexpression of AS160 protein levels in EDL muscle; however, it does not affect GLUT5 protein levels. Therefore, it seems that endurance training plays a role in modulating the damaging effects of diabetes in skeletal muscles through mechanisms other than increasing GLUT5, such as changes in AS160.
Subject:
داخلی
Received: 2024/08/31 | Accepted: 2024/11/23 | Published: 2024/10/31
Received: 2024/08/31 | Accepted: 2024/11/23 | Published: 2024/10/31
Send email to the article author
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
