title: Improved hepatic lipid composition following short-term exercise in nonalcoholic fatty liver disease.
abstract: BACKGROUND
  Hepatic steatosis, insulin resistance, inflammation, low levels of polyunsaturated lipids, and adiponectin are implicated in the development and progression of nonalcoholic fatty liver disease (NAFLD).
  
  
  OBJECTIVE
  We examined the effects of short-term aerobic exercise on these metabolic risk factors.
  
  
  METHODS
  Obese individuals (N = 17, 34.3 ± 1.0 kg/m²) with clinically confirmed NAFLD were enrolled in a short-term aerobic exercise program that consisted of 7 consecutive days of treadmill walking at ~85% of maximal heart rate for 60 minutes per day. Preintervention and postintervention measures included hepatic triglyceride content, and a lipid saturation index and polyunsaturated lipid index (PUI) of the liver, obtained by (1)H magnetic resonance spectroscopy (N = 14). Insulin sensitivity was estimated from an oral glucose tolerance test (OGTT), and mononuclear cells were isolated to assess reactive oxygen species production during the OGTT. Circulating glucose, insulin, and high molecular weight (HMW) adiponectin were determined from plasma.
  
  
  RESULTS
  Short-term aerobic exercise training improved hepatic lipid composition in patients with NAFLD.
  
  
  RESULTS
  Exercise training resulted in an increase in liver PUI (P < .05), increased insulin sensitivity (Matsuda Index: P < .05), HMW adiponectin (P < .05), and maximal oxygen consumption (P < .05). Reactive oxygen species production during the OGTT was reduced following exercise training (P < .05). HMW adiponectin was increased after the exercise program and the increase was positively correlated with the increase in liver PUI (r = 0.52, P = .05). Body weight remained stable during the program (P > .05).
  
  
  CONCLUSIONS
  Short-term exercise can target hepatic lipid composition, which may reduce the risk of NAFLD progression. The improvement in hepatic lipid composition may be driven by adiponectin.
authors.affiliation: Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA.
authors.forename: Jacob M
authors.initials: JM
authors.lastname: Haus
authors.forename: Thomas P J
authors.initials: TP
authors.lastname: Solomon
authors.forename: Karen R
authors.initials: KR
authors.lastname: Kelly
authors.forename: Ciaran E
authors.initials: CE
authors.lastname: Fealy
authors.forename: Emily L
authors.initials: EL
authors.lastname: Kullman
authors.forename: Amanda R
authors.initials: AR
authors.lastname: Scelsi
authors.forename: Lan
authors.initials: L
authors.lastname: Lu
authors.forename: Mangesh R
authors.initials: MR
authors.lastname: Pagadala
authors.forename: Arthur J
authors.initials: AJ
authors.lastname: McCullough
authors.forename: Chris A
authors.initials: CA
authors.lastname: Flask
authors.forename: John P
authors.initials: JP
authors.lastname: Kirwan
mesh_terms: D052242:Adiponectin / Q000097:blood / Q000737:chemistry / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D015992:Body Mass Index; D015444:Exercise; D005234:Fatty Liver / Q000453:epidemiology / Q000209:etiology / Q000517:prevention & control*; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D050152:Intra-Abdominal Fat / Q000276:immunology / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism; D050356:Lipid Metabolism; D008099:Liver / Q000276:immunology / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D008970:Molecular Weight; D009043:Motor Activity; D065626:Non-alcoholic Fatty Liver Disease; D009765:Obesity / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D009820:Ohio / Q000453:epidemiology; D018384:Oxidative Stress; D012307:Risk Factors; D014280:Triglycerides / Q000378:metabolism; D016138:Walking
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D015415:Biomarkers; D014280:Triglycerides