اثر تمرین مقاومتی بر مقدار آنزیمهای آنتیاکسیدانی بافت کبدی در موش صحرایی نر ویستار مبتال به کبد چرب غیرالکلی. (Persian)

Introduction: The pathogenic mechanism underlying non-alcoholic fatty liver disease (NAFLD) and progression from non-alcoholic fatty liver (NAFL) to non-alcoholic steatohepatitis (NASH) is not entirely understood. The purpose of this study was to determine the effect of resistance training on the level of antioxidant enzymes in liver tissue of male Wistar rats with non-alcoholic fatty liver. Materials and Methods: In the present experimental study, 21 adult male Wistar rats were purchased and randomly divided into three groups: control, high fat diet and high fat diet+ resistance training groups. Animals in the high-fat diet groups received a high-fat diet including a combination of fructose, carbon tetrachloride and olive oil for 23 weeks. The training group while receiving a high-fat diet, in the final 8 weeks performed the progressive resistance training protocol including carrying weights equivalent to 30 to 100 percent of body weight three sessions a week. At the end of the intervention, level of superoxide dismutase (SOD) and glutathione peroxidase (GPX) enzymes in liver tissue were measured by enzyme colorimetric method. Also, liver histopathology was performed to confirm the biochemical results. The data collected were analyzed using statistical tests of one-way analysis of variance and Tukey's follow-up test. Results: Liver SOD enzyme level in the high-fat diet+ resistance training group showed significant increase in compared to the high-fat diet group (p = 0.035), but liver GPX enzyme level did not change significantly in the three groups (p = 0.085). The histopathological examination of the liver also confirmed the changes caused by the high-fat diet and the protective effects of resistance training. Conclusion: According to the results of this study, it can be said that resistance training can significantly improve the disorder of antioxidant enzymes and liver tissue steatosis caused by high-fat diet in male Wistar rats with non-alcoholic fatty liver. [ABSTRACT FROM AUTHOR]

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