title: UCP1 -3826 AG+GG genotypes, adiponectin, and leptin/adiponectin ratio in severe obesity.
abstract: OBJECTIVE
  Non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome (MS) are well-recognized complications of obesity. This study was designed to evaluate the role of the UCP1 -3826 A>G polymorphism, adiponectin levels, leptin/adiponectin ratio (L/A), and main biochemical parameters in 102 unrelated severely obese adults [61 females and 41 males, median body mass index (BMI) = 47.8 kg/m2] with NAFLD, with (MS+) or without MS (MS-) from Southern Italy.
  
  
  METHODS
  The UCP1 polymorphism was tested by the TaqMan method, main biochemical parameters by routinary methods, adiponectin, and leptin serum levels by enzyme-linked immunosorbent assay. MS was diagnosed according to the American Heart Association criteria, liver steatosis was detected by ultrasound.
  
  
  RESULTS
  MS was present in 53% male and 66% female obese patients. Only total cholesterol (p=0.04 males and p=0.002 females) and L/A ratio (p=0.03 males) differed between MS+ and MS- obese patients. At multivariate analysis, severe liver steatosis was significantly associated with: UCP1 (AG+GG) genotypes [odds ratio-confidence interval (OR-CI): 4.25; 1.12-16.13], MS (OR-CI: 8.47; 1.78-40.25), low adiponectin levels (OR-CI: 0.92; 0.87-0.98), high alanine aminotransferase levels (OR-CI: 1.03; 1.00-1.06), age (ORCI: 1.08; 1.00-1.15), and male gender (OR-CI: 10.78; 1.61- 71.96).
  
  
  CONCLUSIONS
  In addition to traditional factors, total cholesterol and L/A ratio appear to contribute to MS characterization in severe obesity. Furthermore, the UCP1 (AG+GG) genotypes and low adiponectin levels could predispose to a more severe liver steatosis independently of MS presence. Based on our data, polymorphic UCP1 (AG+GG) obese patients with low adiponectin levels appear to be high-risk subjects for worsening of liver steatosis, a NAFLD, possibly requiring a second-step evaluation by liver biopsy.
authors.affiliation: CEINGE Biotecnologie Avanzate S.C. a R.L., Naples, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Labruna
authors.forename: F
authors.initials: F
authors.lastname: Pasanisi
authors.forename: C
authors.initials: C
authors.lastname: Nardelli
authors.forename: G
authors.initials: G
authors.lastname: Tarantino
authors.forename: D F
authors.initials: DF
authors.lastname: Vitale
authors.forename: R
authors.initials: R
authors.lastname: Bracale
authors.forename: C
authors.initials: C
authors.lastname: Finelli
authors.forename: M P
authors.initials: MP
authors.lastname: Genua
authors.forename: F
authors.initials: F
authors.lastname: Contaldo
authors.forename: L
authors.initials: L
authors.lastname: Sacchetti
mesh_terms: D052242:Adiponectin / Q000097:blood / Q000378:metabolism*; D000293:Adolescent; D000328:Adult; D000368:Aged; D000410:Alanine Transaminase / Q000097:blood; D001219:Aspartate Aminotransferases / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D002784:Cholesterol / Q000097:blood; D005234:Fatty Liver / Q000097:blood / Q000235:genetics / Q000378:metabolism; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood; D007473:Ion Channels / Q000235:genetics* / Q000378:metabolism; D007558:Italy; D020738:Leptin / Q000097:blood / Q000378:metabolism*; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000235:genetics / Q000378:metabolism; D008875:Middle Aged; D024101:Mitochondrial Proteins / Q000235:genetics* / Q000378:metabolism; D009767:Obesity, Morbid / Q000097:blood / Q000235:genetics* / Q000378:metabolism*; D020641:Polymorphism, Single Nucleotide; D018709:Statistics, Nonparametric; D014280:Triglycerides / Q000097:blood; D000071256:Uncoupling Protein 1; D055815:Young Adult; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D007328:Insulin; D007473:Ion Channels; D020738:Leptin; D024101:Mitochondrial Proteins; D014280:Triglycerides; C000604371:UCP1 protein, human; D000071256:Uncoupling Protein 1; D002784:Cholesterol; D005723:gamma-Glutamyltransferase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase