title: Contribution of the cholesteryl ester transfer protein gene TaqIB polymorphism to the reduced plasma HDL-cholesterol levels found in abdominal obese men with the features of the insulin resistance syndrome.
abstract: OBJECTIVE
  The aim of this study was to examine the relation between the CETP-TaqIB polymorphism and reduced plasma HDL-cholesterol levels commonly observed among men characterized by abdominal obesity and features of the insulin resistance syndrome.
  
  
  METHODS
  A total of 187 sedentary men, non-smokers and free from metabolic disorders were classified on the basis of their CETP-TaqIB genotype.
  
  
  RESULTS
  Plasma HDL and HDL3-cholesterol concentrations as well as the CETP activity were significantly different between the three genotypes, B1B1 men having significantly lower HDL and HDL3-cholesterol levels and higher CETP activity than B2B2 homozygotes. A 2x3 ANOVA was used to determine the source of variation of plasma HDL and HDL2-cholesterol levels among the three genotypic groups of men divided on the basis of either a high (>/=27 kg/m2) or a low (<27 kg/m2) BMI, a high (>/=130 cm2) or a low (<130 cm2) accumulation of visceral adipose tissue assessed by computed tomography, or a low versus a high fasting plasma insulin concentration (using the median value as a cut-off point). The effect of the CETP genotype observed on plasma HDL-cholesterol concentrations was attenuated among men with features of the insulin resistance syndrome. It seems that the expected raising effect of the B2 allele on plasma HDL-cholesterol concentrations was blunted in the presence of a BMI>/=27 kg/m2, a high accumulation of visceral adipose tissue or hyperinsulinaemia.
  
  
  CONCLUSIONS
  Our data indicate that the CETP gene TaqIB polymorphism influences plasma CETP activity on one hand and plasma HDL-cholesterol concentrations on the other hand among men. The association between the TaqIB polymorphism and plasma HDL-cholesterol concentrations is altered by the presence of abdominal obesity and some features of the insulin resistance syndrome.
authors.affiliation: Lipid Research Center, Québec, Canada.
authors.forename: M C
authors.initials: MC
authors.lastname: Vohl
authors.forename: B
authors.initials: B
authors.lastname: Lamarche
authors.forename: A
authors.initials: A
authors.lastname: Pascot
authors.forename: G
authors.initials: G
authors.lastname: Leroux
authors.forename: D
authors.initials: D
authors.lastname: Prud'homme
authors.forename: C
authors.initials: C
authors.lastname: Bouchard
authors.forename: A
authors.initials: A
authors.lastname: Nadeau
authors.forename: J P
authors.initials: JP
authors.lastname: Després
mesh_terms: D000005:Abdomen; D000273:Adipose Tissue / Q000033:anatomy & histology*; D000328:Adult; D000704:Analysis of Variance; D002352:Carrier Proteins / Q000235:genetics*; D053480:Cholesterol Ester Transfer Proteins; D008076:Cholesterol, HDL / Q000097:blood* / Q000235:genetics; D004247:DNA / Q000032:analysis; D005951:Glucose Tolerance Test; D006023:Glycoproteins; D006801:Humans; D007333:Insulin Resistance; D008297:Male; D009765:Obesity / Q000097:blood / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011792:Quebec; D044465:White People / Q000235:genetics
chemical_list: C506642:CETP protein, human; D002352:Carrier Proteins; D053480:Cholesterol Ester Transfer Proteins; D008076:Cholesterol, HDL; D006023:Glycoproteins; D004247:DNA