Tag Archives: mitofusin
The effects of endurance training and estrogen-related receptor α disruption on mitofusin 1 and 2, GLUT2, PPARβ/δ and SCD1 expression in the liver of diabetic rats
B. Shahouzehi1,2, Y. Masoumi-Ardakani3, H. Fallah4, S. Aminizadeh3*
1Student Research Committee, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran;
2Cardiovascular Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran;
3Physiology Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran;
4Department of Biochemistry, Afzalipour School of Medicine, Kerman University of Medical Sciences, Kerman, Iran;
*e-mail: soheilaminizadeh@gmail.com
Received: 19 March 2020; Accepted: 13 November 2020
Diabetes is a progressive and metabolic disease with a high prevalence throughout the world. Physical activity is considered as an intervention to improve diabetes. Intervention such as estrogen-related receptor α (ERRα) inhibition is considered as a new way to manage diabetes. In current study, we examined ERRα inhibition along with exercise training (ET) on the gene expression of mitofusin 1 (MFN1), MFN2, glucose transporter 2 (GLUT2), peroxisome proliferator-activated receptor beta or delta (PPARβ/δ), and stearoyl-CoA desaturase 1 (SCD1) in rat liver. The animals were divided into 8 groups (n = 7); 1, Control (CTL) 2, Diabetes (D) 3, ERRα inhibition (ERRI) 4, Endurance Training (ET) 5, Diabetes+ERRα inhibition (D+ERRI) 6, Diabetes+Endurance training (D+ET) 7, Endurance Training +ERRα inhibition (ET+ERRI) 8, Diabetes+Endurance Training+ERRα inhibition (D+ET+ERRI). The liver tissues were used for Real-Time PCR. The results showed that ET significantly increased PPARδ, MFN1 and, MFN2 expression in control rats compared to DM group. In ERRI group, SCD1, GLUT2, MFN1 and MFN2 gene expression was increased compared to CTL and D group. In CTL and D rats, the combination of ERRα inhibition and ET significantly and additively increased MFN1, MFN2, and GLUT2 expression. Overall, the combination of ET and ERRα inhibition probably can be considered as a potential therapeutic intervention for treatment of metabolic diseases including diabetes and cardiovascular disease.