title: Regular exercise coupled to diet regimen accelerates reduction of hepatic steatosis and associated pathological conditions in nonalcoholic fatty liver disease.
abstract: BACKGROUND
  A diet regimen focusing on weight loss is still the most efficient treatment for nonalcoholic fatty liver disease (NAFLD). Recently, specific benefits of exercise against NAFLD independent of weight loss have been reported. Hence, combining exercise with diet-induced weight loss can be expected to have an additive benefit for NAFLD management. We evaluated the effectiveness of diet in conjunction with exercise (DE) compared with that of diet alone (D) on hepatic steatosis and its underlying pathophysiology.
  
  
  METHODS
  Data obtained from 72 obese, middle-aged men with NAFLD who completed a 3-month program of DE or D in 2011 and 2012 were analyzed. Subjects went through a comprehensive parameters analysis for the pathophysiology of NAFLD.
  
  
  RESULTS
  Subjects in the DE group, compared with those in the D group, elicited additive effects on the degree of hepatic steatosis (-82.6% vs. -60.0%) and body weight (-13.3% vs. -8.9%) accompanied by an improvement in serum marker levels: inflammation, ferritin (-16.1% vs. -2.1%); oxidative stress, lipid peroxidation (-31.8% vs. +4.8%); adipokine imbalance, adiponectin, and leptin (+27.4% vs. +2.6% and -74.4% vs. -30.2%). Consequently, subjects in the DE group achieved further attenuation of insulin resistance [homeostatsis model assessment of insulin resistance (HOMA-IR) (-63.6% vs. -40.0%)]. These observed additive benefits in the DE group were closely associated with the increased volume of physical activity.
  
  
  CONCLUSIONS
  The addition of exercise to a diet regimen potentiates the benefits in NAFLD management through further improvement of hepatic steatosis, inflammatory and oxidative stress levels, and adipokine imbalance, thereby attenuating insulin resistance independent of detectable weight loss.
authors.affiliation: 1 Sports Medicine, Graduate School of Comprehensive Human Sciences, University of Tsukuba , Tsukuba, Ibaraki, Japan .
authors.forename: Sechang
authors.initials: S
authors.lastname: Oh
authors.forename: Kiyoji
authors.initials: K
authors.lastname: Tanaka
authors.forename: Takehiko
authors.initials: T
authors.lastname: Tsujimoto
authors.forename: Rina
authors.initials: R
authors.lastname: So
authors.forename: Takashi
authors.initials: T
authors.lastname: Shida
authors.forename: Junichi
authors.initials: J
authors.lastname: Shoda
mesh_terms: D054392:Adipokines / Q000097:blood; D052242:Adiponectin / Q000097:blood; D050154:Adiposity; D000328:Adult; D000368:Aged; D000886:Anthropometry; D015992:Body Mass Index; D004032:Diet; D004038:Diet, Reducing; D015444:Exercise; D005234:Fatty Liver / Q000150:complications / Q000628:therapy*; D005293:Ferritins / Q000097:blood; D006801:Humans; D007249:Inflammation; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood; D015227:Lipid Peroxidation; D008099:Liver / Q000473:pathology; D008297:Male; D008875:Middle Aged; D065626:Non-alcoholic Fatty Liver Disease / Q000150:complications / Q000628:therapy*; D009765:Obesity / Q000150:complications; D018384:Oxidative Stress
chemical_list: D054392:Adipokines; D052242:Adiponectin; D020738:Leptin; D005293:Ferritins