title: Plasma adiponectin is decreased in nonalcoholic fatty liver disease.
abstract: OBJECTIVE
  Nonalcoholic fatty liver disease (NAFLD) is a major cause of liver-related morbidity and is frequently associated with obesity and metabolic syndrome. The recently discovered hormone adiponectin is produced by adipose tissue, and low plasma adiponectin is considered a key factor in the development of the insulin resistance underlying metabolic syndrome. Animal studies suggest that adiponectin may protect against non-alcoholic steatohepatitis, but direct evidence in humans is lacking. We therefore conducted this study to assess the relationship between plasma adiponectin and nonalcoholic fatty liver disease to explore its role in the pathogenesis of this disease.
  
  
  METHODS
  We measured plasma adiponectin and anthropometric, biochemical, hormonal and metabolic correlates in a group of 17 NAFLD patients with diagnosis confirmed by biopsy, and 20 controls with comparable age, body-mass index and sex. Furthermore we compared plasma adiponectin in patients with simple steatosis and steatohepatitis.
  
  
  RESULTS
  Plasma adiponectin was significantly lower in NAFLD patients than controls (5.93+/-0.45 vs 15.67+/-1.60ng/ml). Moreover, NAFLD patients were significantly more insulin resistant while having similar serum leptin. Adiponectin was similar in simple steatosis and in steatohepatitis (6.16+/-0.78 vs 5.69+/-0.49ng/ml). An inverse correlation was observed between adiponectin and homeostatic model assessment (HOMA) of insulin resistance (P = 0.008), while adiponectin did not correlate with serum transaminases and lipid values.
  
  
  CONCLUSIONS
  These data support a role for low circulating adiponectin in the pathogenesis of NAFLD and confirm the strict association between reduced adiponectin production by adipose tissue, NAFLD and insulin resistance.
authors.affiliation: Endocrine-Metabolic Laboratory, Department of Medical and Surgical Sciences, University of Padova, Padova, Italy. claudio.pagano@unipd.it
authors.forename: Claudio
authors.initials: C
authors.lastname: Pagano
authors.forename: Giorgio
authors.initials: G
authors.lastname: Soardo
authors.forename: Walter
authors.initials: W
authors.lastname: Esposito
authors.forename: Francesco
authors.initials: F
authors.lastname: Fallo
authors.forename: Lorenza
authors.initials: L
authors.lastname: Basan
authors.forename: Debora
authors.initials: D
authors.lastname: Donnini
authors.forename: Giovanni
authors.initials: G
authors.lastname: Federspil
authors.forename: Leonardo A
authors.initials: LA
authors.lastname: Sechi
authors.forename: Roberto
authors.initials: R
authors.lastname: Vettor
mesh_terms: D052242:Adiponectin; D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D000469:Alkaline Phosphatase / Q000097:blood; D001219:Aspartate Aminotransferases / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism*; D008076:Cholesterol, HDL / Q000097:blood; D005234:Fatty Liver / Q000097:blood*; D005260:Female; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood*; D020738:Leptin / Q000097:blood; D008297:Male; D015999:Multivariate Analysis; D012044:Regression Analysis; D014280:Triglycerides / Q000097:blood; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D008076:Cholesterol, HDL; D007328:Insulin; D036341:Intercellular Signaling Peptides and Proteins; D020738:Leptin; D014280:Triglycerides; D005723:gamma-Glutamyltransferase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D000469:Alkaline Phosphatase