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Khayampour N, Peeri M, Azarbayjani M A, Delfan M. Effects of High Intensity Interval Training on the Gene Expression of PGC1-Α, CS and P-53 in the Cardiomyocyte of Male Obese Rats in Type 2 Diabetes. JSSU 2021; 28 (11) :3215-3225
URL: http://jssu.ssu.ac.ir/article-1-5168-en.html

Introduction: Exercise training with different intensity regulates metabolism at the cellular level by regulating the expression of genes involved in mitochondrial biogenesis in diabetic patients. The aim of this study was to evaluate the effect of 4 weeks of high intensity interval training on the expression of PGC-1α, CS and p-53 genes in the cardiomyocytes of obese male rats with type 2 diabetes.
Methods: The present study was an experimental one. Eighteen obese male diabetic rats were divided into three groups of six: high intensity interval training (HIIT), diabetic control (DC), healthy control (NC). Diabetes was induced in all groups except the healthy control group by streptozotocin (STZ) injection. After anesthesia, blood serum was obtained directly from their left ventricle and immediately extracted from their left ventricle. Plasma glucose was measured by glucose oxidase assay. To determine the expression of PGC-1α, CS and P-53 genes, PCR-Real time method and group comparison were used by one-way ANOVA test with application 8 version  graph pad prism at alpha level of 0.05.
Results: The increase in PGC-1α gene expression in HIIT group compared to DC (P = 0.0001) and NC (P = 0.001) groups was significant. Increased expression of CS gene in HIIT group was significant compared to DC (P = 0.0001) and NC (P = 0.009) groups. Decreased expression of P-53 gene in HIIT group compared to DC (P = 0.0001) and NC (P = 0.001) groups were significantly different. Weight and glucose were significantly reduced in the HIIT group.
Conclusion: The results showed that by increasing the PGC-1α, CS genes and decreasing the expression of P-53 gene in cardiomyocytes of obese diabetic rats, it improves the energy metabolism in diabetic patients due to mitochondrial deficiency and possibly it can improve diabetic cardiomyopathy.