The hypolipidemic of ten weeks exercise training on dexamethasone-induced non-alcoholic liver fatty disease in male rats

Oral Presentation
Paper ID : 1817-12THCONG
Oral / Poster Presentation File: 1817-12THCONG.mp4 
Authors
1Department of Exercise Physiology, Faculty of Sport Sciences, University of Mazandaran, Babolsar, Iran
2Department of Physiology, School of Veterinary Medicine, Shiraz University, Shiraz, Iran
Abstract
Abstract
In the past two decades, non-alcoholic fatty liver disease (NAFLD) has emerged as the most prevalent form of chronic liver disease, affecting globally, and increases the risk of incident obesity, type 2 diabetes, and insulin resistance. Overnutrient-induced chronic metabolic diseases, as the hallmarks of the 21st century’s public health, are growing threats worldwide. NAFLD begins with the excessive triglyceride accumulation in hepatocytes, and develops to hepatocellular steatosis with inflammation. The liver is the central mediator of lipid metabolism by regulation of fatty acid (FA) uptake, manufacture, store, export, and oxidation in response to physiological fluctuations of nutrients. Exercise training ameliorates nonalcoholic fatty liver disease (NAFLD) as well as obesity and metabolic syndrome. The exact mechanisms of anti-hyperlipidemic effects of exercise training are not fully understood. The aim of this study was to evaluate the anti- hyperlipidemic effects of exercise training on NAFLD induced by dexamethasone (DEX) in male rats. Twenty- four adult male Sprague-Dawley rats were randomly divided into four groups and trained 5daye in weeks for 10 weeks (65% VO2max). At the end of the study, serum levels of liver enzymes, lipid profiles and blood glucose were measured. The results showed that DEX could significantly change the level of lipid profiles, liver enzymes and blood glucose in rats with NAFLD compared to control group (p<0.05), while 10 weeks training exercise in patient rats could significantly ameliorate them (p<0.05). The molecular results also showed that DEX significantly up-regulated the hepatic expression of SREBP-1c (p<0.05); while, 10 weeks training exercise in patient rats could significantly ameliorate them compared to rats with NAFLD (p<0.05). It can be concluded that t 10 weeks training exercise could alleviate DEX-induced NAFLD through improving lipid metabolism.
Keywords
Subjects