title: Beneficial mechanisms of aerobic exercise on hepatic lipid metabolism in non-alcoholic fatty liver disease.
abstract: BACKGROUND
  Non-alcoholic fatty liver disease (NAFLD) refers to any fatty liver disease that is not due to excessive use of alcohol. NAFLD probably results from abnormal hepatic lipid metabolism and insulin resistance. Aerobic exercise is shown to improve NAFLD. This review aimed to evaluate the molecular mechanisms involved in the beneficial effects of aerobic exercise on NAFLD.
  
  
  METHODS
  We searched articles in English on the role of aerobic exercise in NAFLD therapy in PubMed.
  
  
  RESULTS
  The mechanisms of chronic aerobic exercise in regulating the outcome of NAFLD include: (i) reducing intrahepatic fat content by down-regulating sterol regulatory element-binding protein-1c and up-regulating peroxisome proliferator-activated receptor gamma expression levels; (ii) decreasing hepatic oxidative stress through modulating the reactive oxygen species, and enhancing antioxidant enzymes such as catalase and glutathione peroxidase; (iii) ameliorating hepatic inflammation via the inhibition of pro-inflammatory mediators such as tumor necrosis factor-alpha and interleukin-1 beta; (iv) attenuating mitochondrial dependent apoptosis by reducing cytochrome C released from the mitochondria to the cytosol; and (v) inducing hepato-protective autophagy.
  
  
  CONCLUSIONS
  Aerobic exercise, via different mechanisms, significantly decreases the fat content of the liver and improves the outcomes of patients with NAFLD.
authors: Departments of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. tgeorge@hku.hk.
authors: Rui
authors: R
authors: Guo
authors: Emily C
authors: EC
authors: Liong
authors: Kwok Fai
authors: KF
authors: So
authors: Man-Lung
authors: ML
authors: Fung
authors: George L
authors: GL
authors: Tipoe
mesh_terms: D017209:Apoptosis; D001343:Autophagy; D045304:Cytochromes c / Q000378:metabolism; D015536:Down-Regulation; D015444:Exercise / Q000502:physiology*; D006505:Hepatitis / Q000517:prevention & control; D006801:Humans; D053583:Interleukin-1beta / Q000037:antagonists & inhibitors; D050152:Intra-Abdominal Fat; D050356:Lipid Metabolism / Q000502:physiology*; D008099:Liver / Q000378:metabolism*; D008928:Mitochondria / Q000378:metabolism; D065626:Non-alcoholic Fatty Liver Disease / Q000201:enzymology / Q000378:metabolism*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D051780:Sterol Regulatory Element Binding Protein 1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D053583:Interleukin-1beta; D017382:Reactive Oxygen Species; D051780:Sterol Regulatory Element Binding Protein 1; D014409:Tumor Necrosis Factor-alpha; D045304:Cytochromes c