THE EFFECT OF ENDURANCE TRAINING ON PROTEIN KINASE-B AND MECHANICAL TARGET OF RAPAMYCIN IN THE LEFT VENTRICLE OF THE HEART OF DIABETIC RATS INDUCED BY STREPTOZOTOCIN AND NICOTINAMIDE

نویسندگان

  • Moghaddami, Kamilia Department of Pure and Basic Science, Hashtgerd Branch, Islamic Azad University, Alborz, Iran
  • Shabani, Maryam Department of Pure and Basic Science, Hashtgerd Branch, Islamic Azad University, Alborz, Iran
  • Sherafati Moghadam, Mohammad Department of Pure and Basic Science, Hashtgerd Branch, Islamic Azad University, Alborz, Iran
چکیده مقاله:

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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عنوان ژورنال

دوره 19  شماره 6

صفحات  309- 317

تاریخ انتشار 2020-08

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