Document Type : Original Article

Authors

1 PhD Student in Exercise Physiology, Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Guilan, Rasht, Iran.

2 Professor at Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Guilan, Rasht, Iran.

3 Associate Professor at Department of Biochemistry, Faculty of Sciences, University of Guilan, Rasht, Iran.

4 Assistant Professor at Department of Biotechnology, Faculty of Agricultural Sciences, University of Guilan, Rasht, Iran.

Abstract

Background and Aim: The study of lipid formation and degradation in response to dietary and exercise stimuli may provide a better perspective for preventing and treating nonalcoholic fatty liver disease. Therefore, this study aims to investigate the effects of diet, exercise, and hypoxia on the molecular mechanisms related to lipid metabolism. Materials and Methods: A total of twenty-four male Wistar rats aged approximately five weeks with an average weight of 165.9±9.94 grams were randomly divided into four groups including normal diet (ND), high-fat diet (HFD), high-fat diet+exercise in normoxia (HFD+NE), and high-fat diet+exercise in hypoxia (HFD+HE). The maximal aerobic velocity (MAV) was determined under normoxic conditions (at an altitude of approximately 50 m) and hypoxic-hypobaric conditions (at an altitude of approximately 3000 m). Following this, considering overload, exercise sessions were conducted three times a week for a duration of 12 weeks at intensities ranging from 68 to 80 percent of MAV.  At the end, tissue samples were collected to measure changes in the expression of Srebf1, Chreb and Atgl genes. Gene expression was measured using Real-Time PCR method and data were analyzed using ANOVA and Tukey tests at a significance level of p<0.05. Results: The results showed that in all groups receiving a HFD, liver fat content and expression of Srebf1 and Chreb, genes were increased; whereas the increase in Srebf1 and Chreb was greater in the HFD+HE group than in the other groups. Moreover, Atgl gene expression was lower in the HFD group than in other groups. Conclusion: A HFD apparently increases liver fat content by increasing lipogenesis and decreasing lipolysis. Exercise is thought to regulate the increase in liver fat content in rats on HFD by increasing the expression of lipolysis genes. Training probably plays a lesser role than diet in altering lipogenic genes expression than nutrition. Hypoxic training had no additional effect on reducing liver fat content.

Keywords

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