Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/43719
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dc.contributor.authorLópez Ríos,Lauraen_US
dc.contributor.authorPérez-Jiménez, P.en_US
dc.contributor.authorMartínez Quintana, Efrénen_US
dc.contributor.authorRodriguez González, G.en_US
dc.contributor.authorDíaz Chico, Bonifacio Nicolásen_US
dc.contributor.authorNovoa Mogollón,Franciscoen_US
dc.contributor.authorSerra Majem, Luisen_US
dc.contributor.authorChirino Godoy, Ricardoen_US
dc.date.accessioned2018-11-21T17:18:54Z-
dc.date.available2018-11-21T17:18:54Z-
dc.date.issued2011en_US
dc.identifier.issn0939-4753en_US
dc.identifier.urihttp://hdl.handle.net/10553/43719-
dc.description.abstractBACKGROUND AND AIMS: 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. METHODS AND RESULT: 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). CONCLUSION: The observed influence of Taq 1B polymorphism on insulin levels and HOMA highlights the possible role of CETP in the regulation of glucose homeostasis.en_US
dc.languageengen_US
dc.publisher0939-4753-
dc.relation.ispartofNutrition, Metabolism and Cardiovascular Diseasesen_US
dc.sourceNutrition, Metabolism and Cardiovascular Diseases [ISSN 0939-4753], v. 21(1), p. 18-24en_US
dc.subject320501 Cardiologíaen_US
dc.subject.otherTaq 1B polymorphismen_US
dc.subject.otherCETPen_US
dc.subject.otherInsulinen_US
dc.subject.otherHOMAen_US
dc.titleAssociation of Taq 1B CETP polymorphism with insulin and HOMA levels in the population of the Canary Islandsen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.numecd.2009.06.009en_US
dc.identifier.scopus78751630656-
dc.identifier.isi000286461200003-
dc.contributor.authorscopusid33068166900-
dc.contributor.authorscopusid37665747500-
dc.contributor.authorscopusid23485891800-
dc.contributor.authorscopusid55863671600-
dc.contributor.authorscopusid7003603506-
dc.contributor.authorscopusid12786120600-
dc.contributor.authorscopusid35596972100-
dc.contributor.authorscopusid6701324062-
dc.description.lastpage24en_US
dc.identifier.issue1-
dc.description.firstpage18en_US
dc.relation.volume21en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.contributor.daisngid1964185-
dc.contributor.daisngid10057424-
dc.contributor.daisngid614797-
dc.contributor.daisngid4484337-
dc.contributor.daisngid1724161-
dc.contributor.daisngid556390-
dc.contributor.daisngid28836-
dc.contributor.daisngid1922831-
dc.description.numberofpages7en_US
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Lopez-Rios, L-
dc.contributor.wosstandardWOS:Perez-Jimenez, P-
dc.contributor.wosstandardWOS:Martinez-Quintana, E-
dc.contributor.wosstandardWOS:Gonzalez, GR-
dc.contributor.wosstandardWOS:Diaz-Chico, BN-
dc.contributor.wosstandardWOS:Novoa, FJ-
dc.contributor.wosstandardWOS:Serra-Majem, L-
dc.contributor.wosstandardWOS:Chirino, R-
dc.date.coverdateEnero 2011en_US
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.sjr1,357
dc.description.jcr3,731
dc.description.sjrqQ1
dc.description.jcrqQ1
dc.description.scieSCIE
item.grantfulltextopen-
item.fulltextCon texto completo-
crisitem.author.deptDepartamento de Ciencias Médicas y Quirúrgicas-
crisitem.author.deptGIR IUIBS: Bioquímica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología-
crisitem.author.deptGIR IUIBS: Diabetes y endocrinología aplicada-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptGIR IUIBS: Nutrición-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Clínicas-
crisitem.author.deptGIR IUIBS: Diabetes y endocrinología aplicada-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología-
crisitem.author.orcid0000-0002-0944-990X-
crisitem.author.orcid0000-0003-3629-8120-
crisitem.author.orcid0000-0002-9658-9061-
crisitem.author.orcid0000-0002-5681-8931-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameLópez Ríos,Laura-
crisitem.author.fullNameMartínez Quintana, Efrén-
crisitem.author.fullNameDíaz Chico, Juan Carlos-
crisitem.author.fullNameNovoa Mogollón,Francisco-
crisitem.author.fullNameSerra Majem, Luis-
crisitem.author.fullNameChirino Godoy, Ricardo-
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