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Hakim Sabzevari University
Roya Askari, PhD
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Showing 1 results for Mfn-2

Miss Soghra Sujodi, Dr. Maghsoud Peeri, Dr. Parvin Farzanegi, Dr. Maryam Delfan,
Volume 19, Issue 19 (3-2018)

Introduction: Diabetic cardiomyopathy refers to changes in the heart as a result of altered glucose homeostasis, leading to ventricular dysfunction, and it is associated with mitochondrial abnormality. Since physical exercise has been known as cardioprotective, the aim of the present study was to investigate the effect of 6 weeks of resistance exercise preconditioning on mitochondrial fusion and fission processes in cardiac tissue of type 2 diabetic rats.
Methods: 18 male Westar rats were randomly divided into 3 groups: diabetes group (n=6), exercise + diabetes group (n=6) and control group (n=6); The exercise group performed resistance training (Carrying weights with 40 to 160 percent of body weight on the ladder) for 6 weeks and 5 sessions per week. To induce type 2 diabetes, a high-fat diet was administered concurrently with the start of the training program and continued until the end of the study, and 48 hours after the last training session, the injection of STZ was administered intraperitoneally at a dose of 25 mg/kg. Seven days after STZ injection, all rats were dissected and their left ventricular tissue extracted. Real-time-PCR was used to measure the mRNA expression of MFN-2, OPA-1 and Drp-1 genes. Statistical analysis was performed using one-way analysis of variance at a significance level of p ≤ 0.05.
Results: Decreased mRNA expression of MFN-2 and OPA-1 genes and increased mRNA expression of Drp-1 gene were observed in diabetic group animals compared to control ones (p ≥ 0.001). Also, trained diabetic rats showed higher MFN-2 and OPA-1 mRNA expression (p ≥ 0.001), and lower Drp-1 mRNA expression (p ≥ 0.01) compared to the diabetic group.
Conclusion: It seems that 6 weeks of resistance training preconditioning can reduce the risk of diabetic cardiomyopathy through the up-regulation of proteins involved in mitochondrial fusion and down-regulation of enhanced mitochondrial fission in the heart tissue.

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