Volume 28, Issue 11 (1-2022)
RJMS 2022, 28(11): 118-124 |
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:
Zare M S, Sanaei B. The Effect of an Exercise Training Period on Hepatic TNF-α Levels in Aged Rats with Non-Alcoholic Fatty Liver Disease. RJMS 2022; 28 (11) :118-124
URL: http://rjms.iums.ac.ir/article-1-9272-en.html
URL: http://rjms.iums.ac.ir/article-1-9272-en.html
1- PhD in Physical Education and Sports Sciences- Sports Physiology Specialization - Department of Education of Yazd Province, Yazd, Iran
2- PhD of Developmental Biology, Department of Embryology, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran ,b.sanaei91@gmail.com
2- PhD of Developmental Biology, Department of Embryology, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran ,
Abstract: (148 Views)
Background & Aims: The primary aim of the present study was to determine the effect of an 8-week aerobic exercise training program on the levels of tumor necrosis factor-alpha (TNF-α) in the liver tissue of aged rats with non-alcoholic fatty liver disease. Given the central role of inflammation in the progression of NAFLD and the heightened inflammatory status associated with aging, this study sought to clarify whether regular physical activity could effectively attenuate hepatic inflammation in an aged experimental model. Specifically, this research aimed to evaluate the anti-inflammatory potential of continuous aerobic exercise by assessing changes in hepatic TNF-α expression following a structured treadmill training protocol. The selection of TNF-α as the primary outcome variable was based on its well-established involvement in insulin resistance, hepatocellular apoptosis, and the progression from simple steatosis to more advanced stages of NAFLD. By focusing on liver tissue rather than circulating inflammatory markers, this study intended to provide more direct evidence of exercise-induced adaptations at the target organ level. Another important objective of this study was to address the gap in the literature regarding exercise interventions in aged populations with NAFLD. Aging is associated with reduced physiological adaptability, altered immune responses, and diminished regenerative capacity, which may influence the effectiveness of exercise as a therapeutic intervention. Therefore, examining the response of aged liver tissue to aerobic training is crucial for understanding whether exercise remains beneficial under these conditions. Furthermore, this study aimed to contribute to the growing body of evidence supporting lifestyle modifications as a cornerstone in the management of NAFLD. Pharmacological treatments for NAFLD remain limited, and long-term drug use may be associated with adverse effects, particularly in elderly individuals. Exercise, as a low-cost and accessible intervention, has the potential to improve liver health while also conferring systemic benefits, including improved cardiovascular fitness and metabolic control. By utilizing a controlled experimental design and a standardized exercise protocol, this study sought to isolate the specific effects of aerobic training on hepatic TNF-α levels. The findings of this research may help clarify the role of exercise in modulating inflammatory pathways in NAFLD and provide a scientific basis for recommending regular physical activity as part of preventive and therapeutic strategies for elderly individuals at risk of or suffering from NAFLD. Methods: Twenty-one aged Wistar rats (approximately 24 months old, weighing 250–360 g) with NAFLD were randomly divided into three groups: healthy control, NAFLD control, and exercise training. After one week of familiarization with the laboratory environment and treadmill running, the exercise group performed an aerobic continuous training program for 8 weeks, 5 sessions per week. Training intensity gradually increased from 15 m/min for 5 minutes in the first week to 20 m/min for 60 minutes by the fourth week and remained constant thereafter. Data were analyzed using one-way analysis of variance (ANOVA). Results: The findings indicated that 8 weeks of regular aerobic exercise resulted in a significant reduction in hepatic TNF-α levels in aged rats with NAFLD compared to the NAFLD control group. Conclusion: The findings of the present study demonstrated that an 8-week program of regular aerobic exercise significantly reduced TNF-α levels in the liver tissue of aged rats with non-alcoholic fatty liver disease. This result highlights the potent anti-inflammatory effects of aerobic exercise and underscores its potential role in modulating key inflammatory mediators involved in the pathogenesis of NAFLD, particularly in the context of aging. The observed reduction in hepatic TNF-α may be attributed to several physiological mechanisms induced by regular exercise. Aerobic training is known to decrease visceral adiposity, which is a major source of pro-inflammatory cytokines. Additionally, exercise improves insulin sensitivity and enhances mitochondrial efficiency, thereby reducing oxidative stress and subsequent inflammatory signaling. These adaptations collectively contribute to a more favorable hepatic environment and may slow or prevent the progression of NAFLD. Importantly, the results suggest that despite age-related declines in physiological adaptability, the aged liver retains the capacity to respond positively to exercise-induced stimuli. This finding is particularly relevant given the increasing prevalence of NAFLD among elderly populations and the limited availability of effective pharmacological treatments. The ability of exercise to reduce hepatic inflammation without adverse side effects makes it an attractive therapeutic option for older individuals. The present study also reinforces the concept that exercise should be viewed not only as a means of improving physical fitness but also as a targeted intervention capable of influencing molecular and cellular processes within vital organs such as the liver. By reducing TNF-α levels, aerobic exercise may help attenuate insulin resistance, hepatocyte apoptosis, and fibrotic signaling pathways, thereby contributing to improved liver function and overall metabolic health. Nevertheless, certain limitations should be acknowledged. This study focused on a single inflammatory marker, and future research should explore additional cytokines and signaling pathways involved in NAFLD. Moreover, translating findings from animal models to human populations requires caution. Further studies in elderly humans are necessary to confirm the clinical relevance of these results and to determine optimal exercise modalities, intensities, and durations. In conclusion, the results of this study provide strong evidence that regular aerobic exercise exerts significant anti-inflammatory effects on liver tissue in aged rats with NAFLD. These findings support the incorporation of structured physical activity into preventive and therapeutic strategies aimed at managing NAFLD in the aging population and highlight the importance of exercise as a safe and effective non-pharmacological intervention. |
Send email to the article author
