Volume 31, Issue 4 (July 2020)                   Studies in Medical Sciences 2020, 31(4): 282-294 | Back to browse issues page

XML Persian Abstract Print


Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Bagherian M, Banaeifar A, Arshadi S, Azarbayjani M. THE EFFECT OF EXERCISE TYPE ON THE EXPRESSION OF PGC-1A AND HEART TISSUE TRIGLYCERIDE CONTENT IN RATS WITH FATTY LIVER (NAFLD). Studies in Medical Sciences 2020; 31 (4) :282-294
URL: http://umj.umsu.ac.ir/article-1-5114-en.html
Associate Professor Department of Exercise Physiology, South Tehran Branch, Islamic Azad University, Tehran, Iran (Corresponding Author) , alibanaeifar@yahoo.com
Abstract:   (3763 Views)
Background & Aims: PGC-1a is one of the most important regulators of cardiac mitochondrial biogenesis which plays a key role in lipid oxidation processes. The aim of this study was to investigate the effect of low-intensity endurance training and high-intensity interval training on the expression of PGC-1a and heart tissue triglyceride content in rats with fatty liver (NAFLD).
 Materials & Methods: This experimental study was performed on 40 male Wistar rats. Rats were randomly divided into 4 groups. The control group received low-intensity endurance training and intense interval training that consumed high fat diet for 16 weeks and then the two training groups participated in the exercise program for 8 weeks. Also, the sham group used standard food during this time. Finally, expression levels of PGC-1a and intracellular adipose tissue of the four groups were measured.
 Results: The results showed that expression of PGC-1a increased after endurance training and intense interval training in cardiac tissue of obese male rats. Also, both types of intense intermittent exercise and low-intensity endurance training significantly decreased the fat content of cardiac tissue (p<0/05).
Conclusion: The results showed that exercise training can increase the expression of PGC-1a and decrease the triglyceride content of the heart tissue in people with non-alcoholic fatty liver disease, indicating that exercise training can be a non-medicinal treatment for these people to use.
Full-Text [PDF 3484 kb]   (978 Downloads)    
Type of Study: Research | Subject: Exercise physiology

References
1. Masarone, M., et al., Non alcoholic fatty liver: epidemiology and natural history. Reviews on recent clinical trials, 2014. 9(3): p. 126-133. [DOI:10.2174/1574887109666141216111143] [PMID]
2. Federico, A., et al., The epidemiology of non-alcoholic fatty liver disease and its connection with cardiovascular disease: role of endothelial dysfunction. Eur Rev Med Pharmacol Sci, 2016. 20(22): p. 4731-4741. [Google Scholar]
3. Hamaguchi, M., et al., Nonalcoholic fatty liver disease is a novel predictor of cardiovascular disease. W.J.G, 2007. 13(10): p. 1579. [DOI:10.3748/wjg.v13.i10.1579] [PMID] [PMCID]
4. Deurenberg, P., M. Deurenberg‐Yap, and S. Guricci, Asians are different from Caucasians and from each other in their body mass index/body fat per cent relationship. Obesity reviews, 2002. 3(3): p. 141-146. [DOI:10.1046/j.1467-789X.2002.00065.x] [PMID]
5. Crawford, P.A. and J.E. Schaffer, Metabolic stress in the myocardium: adaptations of gene expression. J. M.C. C. 2013. 55: p. 130-138. [DOI:10.1016/j.yjmcc.2012.06.008] [PMID] [PMCID]
6. Qi, D. and B. Rodrigues, Glucocorticoids produce whole body insulin resistance with changes in cardiac metabolism. A. J. Ph-E. M.2007. 292(3): p. E654-E667. [DOI:10.1152/ajpendo.00453.2006] [PMID]
7. Schulze, P.C., K. Drosatos, and I.J. Goldberg, Lipid use and misuse by the heart. Circulation research, 2016. 118(11): p. 1736-1751. [DOI:10.1161/CIRCRESAHA.116.306842] [PMID] [PMCID]
8. Leporn, N.E., D.D. Fouchian, and P.A. McCulloughn, New vistas for the treatment of obesity: turning the tide against the leading cause of morbidity and cardiovascular mortality in the developed world. Reviews in cardiovascular medicine, 1900. 14(1): p. 20-40. [DOI:10.3909/ricm0682] [PMID]
9. Nakanishi, T. and S. Kato, Impact of diabetes mellitus on myocardial lipid deposition: an autopsy study. Pathology-Research and Practice, 2014. 210(12): p. 1018-1025. [DOI:10.1016/j.prp.2014.04.008] [PMID]
10. Park, J.Y., et al., Alteration in metabolic signature and lipid metabolism in patients with angina pectoris and myocardial infarction. PloS one, 2015. 10(8). [DOI:10.1371/journal.pone.0135228] [PMID] [PMCID]
11. Konstantinidis, K., R.S. Whelan, and R.N. Kitsis, Mechanisms of cell death in heart disease. Arteriosclerosis, thrombosis, and vascular biology, 2012. 32(7): p. 1552-1562. [DOI:10.1161/ATVBAHA.111.224915] [PMID] [PMCID]
12. Little, J.P., et al., A practical model of low‐volume high‐intensity interval training induces mitochondrial biogenesis in human skeletal muscle: potential mechanisms. The J. Ph. 2010. 588(6): p. 1011-1022. [DOI:10.1113/jphysiol.2009.181743] [PMID] [PMCID]
13. Rowe, G.C., A. Jiang, and Z. Arany, PGC-1 coactivators in cardiac development and disease. Circulation research, 2010. 107(7): p. 825-838. [DOI:10.1161/CIRCRESAHA.110.223818] [PMID] [PMCID]
14. Lehman, J.J., et al., Peroxisome proliferator-activated receptor γ coactivator-1 promotes cardiac mitochondrial biogenesis. The J.C. 2000. 106(7): p. 847-856. [DOI:10.1172/JCI10268] [PMID] [PMCID]
15. Lira, V.A., et al., Nitric oxide and AMPK cooperatively regulate PGC‐1α in skeletal muscle cells. The J. Ph. 2010. 588(18): p. 3551-3566. [DOI:10.1113/jphysiol.2010.194035] [PMID] [PMCID]
16. Safdar, A., et al., Exercise increases mitochondrial PGC-1α content and promotes nuclear-mitochondrial cross-talk to coordinate mitochondrial biogenesis. J. B. Ch. 2011. 286(12): p. 10605-10617. [DOI:10.1074/jbc.M110.211466] [PMID] [PMCID]
17. Terada, S., et al., Effects of high‐intensity intermittent swimming on PGC‐1α protein expression in rat skeletal muscle. Acta physiologica scandinavica, 2005. 184(1): p. 59-65. [DOI:10.1111/j.1365-201X.2005.01423.x] [PMID]
18. Russell, A.P., et al., Endurance training in humans leads to fiber type-specific increases in levels of peroxisome proliferator-activated receptor-γ coactivator-1 and peroxisome proliferator-activated receptor-α in skeletal muscle. Diabetes, 2003. 52(12): p. 2874-2881. [DOI:10.2337/diabetes.52.12.2874] [PMID]
19. Little, J.P., et al., Acute endurance exercise increases the nuclear abundance of PGC-1α in trained human skeletal muscle. American journal of physiology-regulatory, integrative and comparative physiology, 2010. 298(4): p. R912-R917. [DOI:10.1152/ajpregu.00409.2009] [PMID]
20. Gibala, M.J., et al., Brief intense interval exercise activates AMPK and p38 MAPK signaling and increases the expression of PGC-1α in human skeletal muscle. J. A. Ph. 2009. 106(3): p. 929-934. [DOI:10.1152/japplphysiol.90880.2008] [PMID]
21. Talanian, J.L., et al., Two weeks of high-intensity aerobic interval training increases the capacity for fat oxidation during exercise in women. J. A. Ph. 2007. 102(4): p. 1439-1447. [DOI:10.1152/japplphysiol.01098.2006] [PMID]
22. Motta, V.F., M.B. Aguila, and C.A. Mandarim-de-Lacerda, High-Intensity Interval Training Beneficial Effects in Diet-Induced Obesity in Mice: Adipose Tissue, Liver Structure, and Pancreatic Islets. International Journal of Morphology, 2016. 34(2). [DOI:10.4067/S0717-95022016000200042]
23. Cho, J., et al., Adiponectin mediates the additive effects of combining daily exercise with caloric restriction for treatment of non-alcoholic fatty liver. International J. O. 2016. 40(11): p. 1760-1767. [DOI:10.1038/ijo.2016.104] [PMID]
24. Marcinko, K., et al., High intensity interval training improves liver and adipose tissue insulin sensitivity. Molecular metabolism, 2015. 4(12): p. 903-915. [DOI:10.1016/j.molmet.2015.09.006] [PMID] [PMCID]
25. PITHON-CURI, T.N.C., Aprogram of Moderate Physical Training for Wistar Rats Based on Maximal Oxygen Consumption. Journal of strength and conditioning research, 2007. 21(3): p. 000-000. [DOI:10.1519/R-20155.1] [PMID]
26. Rezaei, R., et al., Effect of eight weeks of continuous and periodic aerobic training on VEGF-A and VEGFR-2 levels of male brain Wistar rats. J. S. Ph. Ph. A. 2015. 16: p. 1221-1213. [URL]
27. Mattijssen, F., et al., Hypoxia-inducible lipid droplet-associated (HILPDA) is a novel peroxisome proliferator-activated receptor (PPAR) target involved in hepatic triglyceride secretion. J. B. Ch. 2014. 289(28): p. 19279-19293. [DOI:10.1074/jbc.M114.570044] [PMID] [PMCID]
28. Suk, M. and Y. Shin, Effect of high-intensity exercise and high-fat diet on lipid metabolism in the liver of rats. J. E. N.B. 2015. 19(4): p. 289. [DOI:10.5717/jenb.2015.15122303] [PMID] [PMCID]
29. Sohrabipour, S., et al., GABA dramatically improves glucose tolerance in streptozotocin-induced diabetic rats fed with high-fat diet. E. J.Ph. 2018. 826: p. 75-84. [DOI:10.1016/j.ejphar.2018.01.047] [PMID]
30. Löfgren, L., G.-B. Forsberg, and M. Ståhlman, The BUME method: a new rapid and simple chloroform-free method for total lipid extraction of animal tissue. Scientific reports, 2016. 6: p. 27688. [DOI:10.1038/srep27688] [PMID] [PMCID]
31. Taylor, C.W., et al., Exercise duration-matched interval and continuous sprint cycling induce similar increases in AMPK phosphorylation, PGC-1α and VEGF mRNA expression in trained individuals. E.J. A. Ph. 2016. 116(8): p. 1445-1454. [DOI:10.1007/s00421-016-3402-2] [PMID] [PMCID]
32. Hoshino, D., et al., High-intensity interval training increases intrinsic rates of mitochondrial fatty acid oxidation in rat red and white skeletal muscle. Applied Physiology, Nutrition, and Metabolism, 2013. 38(3): p. 326-333. [DOI:10.1139/apnm-2012-0257] [PMID]
33. Jung, H.-L. and H.-Y. Kang, Effects of Exercise Intensity on PGC-1α, PPAR-γ, and Insulin Resistance in Skeletal Muscle of High Fat Diet-fed Sprague-Dawley Rats. J. K. S. F. 2014. 43(7): p. 963-971. [DOI:10.3746/jkfn.2014.43.7.963]
34. Duncan, J.G., et al., Rescue of cardiomyopathy in peroxisome proliferator-activated receptor-alpha transgenic mice by deletion of lipoprotein lipase identifies sources of cardiac lipids and peroxisome proliferator-activated receptor-alpha activators. Circulation, 2010. 121(3): p. 426-435. [DOI:10.1161/CIRCULATIONAHA.109.888735] [PMID] [PMCID]
35. Ellison, G.M., et al., Physiological cardiac remodelling in response to endurance exercise training: cellular and molecular mechanisms. Heart, 2012. 98(1): p. 5-10. [DOI:10.1136/heartjnl-2011-300639] [PMID]
36. Tabet, J.-Y., et al., Benefits of exercise training in chronic heart failure. Archives of cardiovascular diseases, 2009. 102(10): p. 721-730. [DOI:10.1016/j.acvd.2009.05.011] [PMID]
37. Ozaki, H., et al., Effects of high-intensity and blood flow-restricted low-intensity resistance training on carotid arterial compliance: role of blood pressure during training sessions. E. J. A. Ph. 2013. 113(1): p. 167-174. [DOI:10.1007/s00421-012-2422-9] [PMID]
38. Charbonneau, A., et al., Alterations in hepatic glucagon receptor density and in Gsα and Giα2 protein content with diet-induced hepatic steatosis: effects of acute exercise. American J .Ph-E. M. 2005. 289(1): p. E8-E14. [DOI:10.1152/ajpendo.00570.2004] [PMID]
39. Kistler, K.D., et al., Physical activity recommendations, exercise intensity, and histological severity of nonalcoholic fatty liver disease. The American journal of gastroenterology, 2011. [DOI:10.1038/ajg.2010.488] [PMID] [PMCID]
40. Stich, V., et al., Adipose tissue lipolysis is increased during a repeated bout of aerobic exercise. J.A. Ph. 2000. 88(4): p. 1277-1283. [DOI:10.1152/jappl.2000.88.4.1277] [PMID]
41. Boutcher, S.H., High-intensity intermittent exercise and fat loss. J. o. 2010. 2011. [DOI:10.1155/2011/868305] [PMID] [PMCID]
42. Hallsworth, K., et al., Modified high-intensity interval training reduces liver fat and improves cardiac function in non-alcoholic fatty liver disease: a randomised controlled trial. Clinical Science, 2015: p. CS20150308. [DOI:10.1042/CS20150308] [PMID]
43. Gibala, M.J. and S.L. McGee, Metabolic adaptations to short-term high-intensity interval training: a little pain for a lot of gain? Exercise and sport sciences reviews, 2008. 36(2): p. 58-63. [DOI:10.1097/JES.0b013e318168ec1f] [PMID]
44. Tremblay, A., J.-A. Simoneau, and C. Bouchard, Impact of exercise intensity on body fatness and skeletal muscle metabolism. Metabolism, 1994. 43(7): p. 814-818. [DOI:10.1016/0026-0495(94)90259-3] [PMID]
45. Mourier, A., et al., Mobilization of visceral adipose tissue related to the improvement in insulin sensitivity in response to physical training in NIDDM: effects of branched-chain amino acid supplements. Diabetes care, 1997. 20(3): p. 385-391. [DOI:10.2337/diacare.20.3.385] [PMID]
46. Weinstein, Y., et al., Reliability of peak-lactate, heart rate, and plasma volume following the Wingate test. Medicine and science in sports and exercise, 1998. 30(9): p. 1456-1460. https://doi.org/10.1097/00005768-199809000-00017 [DOI:10.1249/00005768-199809000-00017] [PMID]
47. Christmass, M.A., B. Dawson, and P.G. Arthur, Effect of work and recovery duration on skeletal muscle oxygenation and fuel use during sustained intermittent exercise. European J. A. Ph . 1999. 80(5): p. 436-447. [DOI:10.1007/s004210050615] [PMID]
48. Bracken, R.M., D.M. Linnane, and S. Brooks, Plasma catecholamine and nephrine responses to brief intermittent maximal intensity exercise. Amino acids, 2009. 36(2): p. 209-217. [DOI:10.1007/s00726-008-0049-2] [PMID]
49. Issekutz Jr, B., Role of beta-adrenergic receptors in mobilization of energy sources in exercising dogs. J. A Ph. 1978. 44(6): p. 869-876. [DOI:10.1152/jappl.1978.44.6.869] [PMID]
50. Crampes, F., et al., Effect of physical training in humans on the response of isolated fat cells to epinephrine. J. A. Ph. 1986. 61(1): p. 25-29. [DOI:10.1152/jappl.1986.61.1.25] [PMID]
51. Trapp, E.G., D.J. Chisholm, and S.H. Boutcher, Metabolic response of trained and untrained women during high-intensity intermittent cycle exercise. American J. . Ph -R. 2007. 293(6): p. R2370-R2375. [DOI:10.1152/ajpregu.00780.2006] [PMID]
52. Bilski, J., et al., Effects of exercise on appetite and food intake regulation. Medicina Sportiva, 2009. 13(2): p. 82-94. [DOI:10.2478/v10036-009-0014-5]

Add your comments about this article : Your username or Email:
CAPTCHA

Send email to the article author


Rights and permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

© 2024 CC BY-NC 4.0 | Studies in Medical Sciences

Designed & Developed by : Yektaweb