Volume 18, Issue 3 (3-2019)
ijdld 2019, 18(3): 116-125 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Aghaei N, Sherafati Moghadam M, Daryanoosh F, Shadmehri S, Jahani Golbar S.
THE EFFECT OF 4 WEEKS’ AEROBIC TRAINING ON THE CONTENT OF MTORC1 SIGNALING PATHWAY PROTEINS IN HEART TISSUE OF TYPE 1 DIABETES RATS
. ijdld 2019; 18 (3) :116-125
URL: http://ijdld.tums.ac.ir/article-1-5814-en.html
URL: http://ijdld.tums.ac.ir/article-1-5814-en.html
Neda Aghaei1 
, Mohammad Sherafati Moghadam2 , Farhad Daryanoosh * 3, Saeedeh Shadmehri4 , Shiva Jahani Golbar4
, Mohammad Sherafati Moghadam2 , Farhad Daryanoosh * 3, Saeedeh Shadmehri4 , Shiva Jahani Golbar4
1- Department of Physical Education and Sport Sciences, Islamic Azad University, AliabadKatoul Branch, Iran
2- Hashtgerd Branch, Islamic Azad University, Alborz, Iran
3- Department of exercise physiology, Faculty of Education and Psychology, University of Shiraz, Iran ,daryanoosh@shirazu.ac.ir
4- Department of Physical Education and Sport Sciences, Islamic Azad University, Yadegar-e-imam Khomeini (RAH) Shahr-e Ray Branch, Tehran, Iran
2- Hashtgerd Branch, Islamic Azad University, Alborz, Iran
3- Department of exercise physiology, Faculty of Education and Psychology, University of Shiraz, Iran ,
4- Department of Physical Education and Sport Sciences, Islamic Azad University, Yadegar-e-imam Khomeini (RAH) Shahr-e Ray Branch, Tehran, Iran
Abstract: (4643 Views)
Background: The mTORC1 pathway is one of the important pathways for protein synthesis in the heart, which can lead to physiological or pathological hypertrophy. Diabetes can lead to defects in this pathway. The aim of this study was to examine the effect of 4 weeks’ aerobic training on the content of mTORC1 signaling pathway proteins in heart tissue of type 1 diabetes rats.
Methods: In this experimental study, 16 Sprague-Dawley male rats (mean weight of 300 ± 20 gr) were selected and after induction of diabetes by STZ was randomly assigned into two groups: diabetic training and diabetic control. The experimental group performed HIIT training for 4 weeks’ accordance with the training program (each session 42 minutes, 10-20 m/m) for 4 weeks, while the control group did not have any training program. Dependent t-test and independent T-test were used to analyze the data
Results: Significant increase was observed in the content of AKT1 (p<0.015), mTOR (p<0.001), P70S6K1 (p<0.006), 4EBP1 (p<0.05) proteins in the aerobic training group compared to control group.
Conclusion: Aerobic training for 4 weeks enabled to activate the pathway AKT1/mTOR/P70S6K1 and AKT1/mTOR/4E-BP1 in mTORC1 pathway; therefore, due to cardiac complications in type 1 diabetic patients, aerobic training can lead to protein synthesis and physiological cardiac hypertrophy through mTORC1 pathway.
Methods: In this experimental study, 16 Sprague-Dawley male rats (mean weight of 300 ± 20 gr) were selected and after induction of diabetes by STZ was randomly assigned into two groups: diabetic training and diabetic control. The experimental group performed HIIT training for 4 weeks’ accordance with the training program (each session 42 minutes, 10-20 m/m) for 4 weeks, while the control group did not have any training program. Dependent t-test and independent T-test were used to analyze the data
Results: Significant increase was observed in the content of AKT1 (p<0.015), mTOR (p<0.001), P70S6K1 (p<0.006), 4EBP1 (p<0.05) proteins in the aerobic training group compared to control group.Conclusion: Aerobic training for 4 weeks enabled to activate the pathway AKT1/mTOR/P70S6K1 and AKT1/mTOR/4E-BP1 in mTORC1 pathway; therefore, due to cardiac complications in type 1 diabetic patients, aerobic training can lead to protein synthesis and physiological cardiac hypertrophy through mTORC1 pathway.
Type of Study: Research |
Subject:
Special
Received: 2018/12/9 | Accepted: 2019/03/18 | Published: 2019/03/15
Received: 2018/12/9 | Accepted: 2019/03/18 | Published: 2019/03/15
Send email to the article author
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
