title: Circulating adiponectin reflects severity of liver disease but not insulin sensitivity in liver cirrhosis.
abstract: BACKGROUND
  The adipocytokine adiponectin has been proposed to play important roles in the regulation of energy homeostasis, insulin sensitivity and shows anti-inflammatory properties.
  
  
  OBJECTIVE
  In this study we investigated the role of circulating adiponectin in different chronic liver diseases, its regulation by systemic anti-tumour necrosis factor (TNF)-alpha treatment and its hepatic metabolism.
  
  
  METHODS
  Plasma adiponectin levels were determined in 87 patients with liver cirrhosis of different aetiologies, seven patients with alcoholic steatohepatitis undergoing systemic anti-TNF-alpha treatment, in 11 patients with liver cirrhosis receiving transjugular intrahepatic portosystemic shunt implantation and in 21 healthy controls.
  
  
  RESULTS
  Adiponectin levels were significantly higher in all subjects with liver cirrhosis of different aetiologies when compared with healthy controls and increased dependent on Child-Pugh classification. In subjects with alcoholic steatohepatitis, systemic anti-TNF-alpha treatment caused a significant decrease in circulating adiponectin. Adiponectin concentrations were similar in portal, hepatic and peripheral veins. No correlation between adiponectin levels and insulin resistance was found in any patient group.
  
  
  CONCLUSIONS
  Our data suggest that circulating adiponectin is increased in liver cirrhosis independent of the aetiology of liver disease. We suggest that high adiponectin levels in chronic liver disease might reflect one of the body's anti-inflammatory mechanisms in chronic liver diseases.
authors.affiliation: Clinical Division of General Internal Medicine, Department of Medicine, Medical University Innsbruck, Austria.
authors.forename: S
authors.initials: S
authors.lastname: Kaser
authors.forename: A
authors.initials: A
authors.lastname: Moschen
authors.forename: A
authors.initials: A
authors.lastname: Kaser
authors.forename: O
authors.initials: O
authors.lastname: Ludwiczek
authors.forename: C F
authors.initials: CF
authors.lastname: Ebenbichler
authors.forename: W
authors.initials: W
authors.lastname: Vogel
authors.forename: W
authors.initials: W
authors.lastname: Jaschke
authors.forename: J R
authors.initials: JR
authors.lastname: Patsch
authors.forename: H
authors.initials: H
authors.lastname: Tilg
mesh_terms: D052242:Adiponectin; D000704:Analysis of Variance; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D016022:Case-Control Studies; D002908:Chronic Disease; D005234:Fatty Liver / Q000097:blood / Q000188:drug therapy / Q000378:metabolism; D005235:Fatty Liver, Alcoholic / Q000097:blood / Q000188:drug therapy / Q000378:metabolism; D005260:Female; D005765:Gastrointestinal Agents / Q000627:therapeutic use; D019694:Hepatitis B, Chronic / Q000097:blood / Q000188:drug therapy / Q000378:metabolism; D019698:Hepatitis C, Chronic / Q000097:blood / Q000188:drug therapy / Q000378:metabolism; D006801:Humans; D000069285:Infliximab; D007333:Insulin Resistance; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood*; D008099:Liver / Q000378:metabolism; D008103:Liver Cirrhosis / Q000097:blood / Q000378:metabolism / Q000601:surgery; D008107:Liver Diseases / Q000097:blood* / Q000378:metabolism; D008297:Male; D019168:Portasystemic Shunt, Transjugular Intrahepatic
chemical_list: D052242:Adiponectin; D000911:Antibodies, Monoclonal; D005765:Gastrointestinal Agents; D036341:Intercellular Signaling Peptides and Proteins; D000069285:Infliximab