Iranian Journal of

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Background: The pathway of insulin messengers is so important that diabetes can lead to disruption of this pathway. However, the aim of this study was to investigate the effect of 8 weeks of endurance training on protein Kinase-B (PKB or AKT) and mechanical target of rapamycin (mTOR) in the left ventricle of the heart of diabetic rats induced by streptozotocin and nicotinamide.
Methods: In this experimental study, 12 head two-month-old Sprague-Dawley rats with a mean weight of 270±20 g were selected. After diabetic induction with streptozotocin and Nicotinamide, rats were randomly assigned to two groups, training and control (6 heads in group each). The rat training program was performed on a treadmill for 8 weeks and 4 sessions per week, including 30 minutes of endurance training with an intensity of about 50 to 70% of the maximum speed. SPSS software and independent t-test were used to analyze the data.
Results: Eight weeks of endurance training resulted in a significant increase in protein Kinase-B content (P=0.03); But no significant change in Protein Mechanistic Target of Rapamycin content was observed in the endurance training group compared to the control (P=0.97).
Conclusion: protein Kinase-B is a key protein for regulating many cellular pathways, which was significantly increased by eight weeks of endurance training. Due to the fact that the content of protein mechanistic target of rapamycin does not change, it is possible that endurance training cannot lead to physiological hypertrophy heart through the mTORC1 pathway.

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Background: AMPK and P53 proteins regulate the TOR protein in the TORC1 complex, which regulates many physiological processes. The aim of this study was to evaluate the effect of AMPK and P53 proteins on the TOR pathway following endurance training in the left ventricle of the heart of diabetic rats by streptozotocin and nicotinamide.
Methods: In this experimental study, 12 head two-month-old Sprague-Dawley rats with a mean weight of 270±20 g were selected. After diabetic induction with streptozotocin and Nicotinamide, rats were randomly assigned to two groups, training and control (6 heads in group each). The training group performed endurance training on a treadmill for rodents for 6 weeks and 4 sessions per week for 42 minutes with an intensity of about 50 to 70% of the maximum speed. SPSS software version 23 and independent t-test were used to analyze the data.
Results: Six weeks of endurance training led to significant increase in the protein content of AMPK (P=0.009) and TOR (P=0.005) between training and control groups in the left ventricular tissue of the heart muscle. In contrast, a significant decrease in P53 protein content was observed between the training and control groups in the left ventricular tissue of the heart muscle (P=0.0001).
Conclusion: The results showed that endurance training can with increase the content of AMPK and TOR proteins and decrease the content of P53 protein to regulate processes such as metabolism, mitochondrial biogenesis, cardiac hypertrophy, inhibition of autophagy in the hearts of diabetic subjects.
 

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Background: Type 2 diabetes is a metabolic disease and the most common endocrine disorder. Visfatin is a cytokine with insulin-mimetic effects which is associated with diabetes. The rs61330082 polymorphism is located in the promoter region of visfatin gene and regulates visfatin gene expression. The aim of this study is to investigate the association of rs61330082 polymorphism of the visfatin gene with biochemical and anthropometric variables, visfatin level, diabetes and insulin resistance.
Methods: This case‑control study was performed on 80 patients with type 2 diabetes and 80 controls (persons without diabetes). Biochemical and anthropometric parameters were determined using standard methods. Insulin and visfatin levels were measured by ELISA method. Genotype was determined by polymerase chain reaction-restriction fragment length polymorphism method. The data was analyzed with SPSS software.
Results: LDL-C level in healthy people and fasting blood sugar level in patients showed a significant difference in carriers of rs61330082 polymorphism genotypes. No associations was found between visfatin level and single nucleotide polymorphism rs61330082 in the current study. Regression analysis showed that genotypes of rs61330082 polymorphism are not significantly associated with type 2 diabetes and insulin resistance.
Conclusion: The rs61330082 polymorphism is associated with LDL-C in healthy subjects and FBS in patients with T2D. Visfatin rs61330082 polymorphism is not associated with visfatin level and type 2 diabetes and insulin resistance.