title: Association of Taq 1B CETP polymorphism with insulin and HOMA levels in the population of the Canary Islands.
abstract: OBJECTIVE
  Cholesteryl ester transfer protein (CETP) is an enzyme with a key role in lipoprotein metabolism. A common genetic polymorphism, the Taq 1B, influences CETP activity and HDL-cholesterol levels, with individual homozygotes for the B1 allele exhibiting higher enzyme activity and lower HDL-cholesterol levels than carriers of at least one B2 allele. Our aim was to analyze the influence of Taq 1B CETP polymorphism on cardiovascular risk factors in a representative sample of adult subjects from Canary population.
  
  
  RESULTS
  A total of 518 adult subjects from the Canary Islands, enrolled in a nutritional survey (the ENCA study), were included. The Taq 1B polymorphism was analyzed by PCR-RFLP. Compared with individuals with at least one B2 allele, and after adjusting for age, sex, BMI, waist perimeter, smoking and alcohol intake, carriers of the B1B1 genotype showed lower HDL-cholesterol levels (geometric mean (95% CI): 46.6 (44.5-48.8) vs. 50.6 (49.1-52.9)mg/dl; P=0.003); and higher insulin (geometric mean (95% CI): 11.1 (10.5-11.9) vs. 10.0 (9.5-10.5μU/ml; P=0.008) and HOMA levels (geometric mean (95% CI): 2.3 (2.1-2.5) vs. 2.1 (1.9-2.1); P=0.009). In addition, the B1B1 genotype was more frequent in individuals who had low levels of HDL-cholesterol according to the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) criteria (Odds Ratio (OR): 1.563; 95% CI: 1.04-2.34; P=0.030), and in those included in the upper quartile of insulinemia (OR: 1.90; 95% CI: 1.20-3.03; P=0.007) and HOMA (OR: 1.61; 95% CI: 1.02-2.57; P=0.043).
  
  
  CONCLUSIONS
  The observed influence of Taq 1B polymorphism on insulin levels and HOMA highlights the possible role of CETP in the regulation of glucose homeostasis.
authors.affiliation: Servicio de Endocrinología, Complejo Hospitalario Universitario Materno Infantil, Las Palmas de Gran Canaria, Spain. drarual@gmail.com
authors.forename: L
authors.initials: L
authors.lastname: López-Ríos
authors.forename: P
authors.initials: P
authors.lastname: Pérez-Jiménez
authors.forename: E
authors.initials: E
authors.lastname: Martínez-Quintana
authors.forename: G
authors.initials: G
authors.lastname: Rodriguez González
authors.forename: B N
authors.initials: BN
authors.lastname: Díaz-Chico
authors.forename: F J
authors.initials: FJ
authors.lastname: Nóvoa
authors.forename: L
authors.initials: L
authors.lastname: Serra-Majem
authors.forename: R
authors.initials: R
authors.lastname: Chirino
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000886:Anthropometry; D001786:Blood Glucose / Q000378:metabolism; D053480:Cholesterol Ester Transfer Proteins / Q000235:genetics*; D008076:Cholesterol, HDL / Q000097:blood / Q000235:genetics; D015331:Cohort Studies; D004247:DNA / Q000235:genetics; D005260:Female; D006706:Homeostasis / Q000235:genetics* / Q000502:physiology*; D006801:Humans; D007328:Insulin / Q000097:blood* / Q000235:genetics*; D007333:Insulin Resistance / Q000235:genetics / Q000502:physiology; D050356:Lipid Metabolism / Q000235:genetics / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009749:Nutrition Surveys; D011110:Polymorphism, Genetic / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013030:Spain / Q000453:epidemiology; D055815:Young Adult
chemical_list: D001786:Blood Glucose; D053480:Cholesterol Ester Transfer Proteins; D008076:Cholesterol, HDL; D007328:Insulin; D004247:DNA