title: The absence of polymorphisms in ADRB3, UCP1, PPARγ, and ADIPOQ genes protects morbid obese patients toward insulin resistance.
abstract: OBJECTIVE
  The insulin resistance (IR) is a major metabolic impairment in severe obesity, a multifactorial disease in which the importance of the effect of single nucleotide polymorphisms (SNP) associations in different rather than individual genes was established. The aim of this study was to test the predictive value of presence/absence of polymorphisms/ variants in β3-adrenergic receptor (ADRB3), uncoupling protein 1 (UCP1), peroxisome proliferator-activated receptor γ (PPARγ), and adiponectin (ADIPOQ) genes in diagnosing the IR in obesity.
  
  
  METHODS
  We studied 112 (40 males, 72 females) severely obese (body mass index: 48.5±7.5 kg/m2) subjects recruited from the outpatient obesity clinic of Federico II University Hospital in Naples. Genomic DNA was extracted from peripheral leukocytes with a commercial kit. The gene polymorphisms Trp64Arg in ADRB3, -3826 A>G in UCP1, Pro12Ala in PPARγ, and c.268G>A, c.331T>C, and c.334C>T in ADIPOQ were characterized by TaqMan assay or by direct sequencing (ADIPOQ).
  
  
  CONCLUSIONS
  Our results demonstrate that -3826A>G UCP1 polymorphism is associated with IR in morbid obesity. Further, the lack of any polymorphisms, Trp64Arg in ADRB3 and/or -3826 A>G in UCP1 and/or Pro12Ala in PPARγ and/or c.268G>A, c.331T>C and c.334C>T in ADIPOQ, appears a useful prognostic factor (NPV=100%) toward the IR onset in these obese patients representing a further parameter for an earlier and appropriate therapy.
authors.affiliation: Dipartimento di Scienze per la Salute, Università del Molise, Campobasso, Italy.
authors.forename: R
authors.initials: R
authors.lastname: Bracale
authors.forename: G
authors.initials: G
authors.lastname: Labruna
authors.forename: C
authors.initials: C
authors.lastname: Finelli
authors.forename: A
authors.initials: A
authors.lastname: Daniele
authors.forename: L
authors.initials: L
authors.lastname: Sacchetti
authors.forename: G
authors.initials: G
authors.lastname: Oriani
authors.forename: F
authors.initials: F
authors.lastname: Contaldo
authors.forename: F
authors.initials: F
authors.lastname: Pasanisi
mesh_terms: D052242:Adiponectin / Q000235:genetics*; D000328:Adult; D001786:Blood Glucose; D015992:Body Mass Index; D004247:DNA / Q000235:genetics; D005260:Female; D006801:Humans; D007328:Insulin; D007333:Insulin Resistance / Q000235:genetics*; D007473:Ion Channels / Q000235:genetics*; D008297:Male; D024101:Mitochondrial Proteins / Q000235:genetics*; D009767:Obesity, Morbid / Q000235:genetics*; D047495:PPAR gamma / Q000235:genetics*; D016133:Polymerase Chain Reaction; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D022702:Receptors, Adrenergic, beta-3 / Q000235:genetics*; D000071256:Uncoupling Protein 1
chemical_list: C499918:ADIPOQ protein, human; C568534:ADRB3 protein, human; D052242:Adiponectin; D001786:Blood Glucose; D007328:Insulin; D007473:Ion Channels; D024101:Mitochondrial Proteins; D047495:PPAR gamma; D022702:Receptors, Adrenergic, beta-3; C000604371:UCP1 protein, human; D000071256:Uncoupling Protein 1; D004247:DNA