Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/43423
Campo DC Valoridioma
dc.contributor.authorLópez-Ríos, Lauraen_US
dc.contributor.authorNóvoa, Francisco J.en_US
dc.contributor.authorChirino Godoy, Ricardoen_US
dc.contributor.authorVarillas, Franciscoen_US
dc.contributor.authorBoronat Cortés, Mauroen_US
dc.contributor.authorWägner, Ana M.en_US
dc.date.accessioned2018-11-21T15:02:45Z-
dc.date.available2018-11-21T15:02:45Z-
dc.date.issued2011en_US
dc.identifier.issn1932-6203en_US
dc.identifier.otherWoS-
dc.identifier.urihttp://hdl.handle.net/10553/43423-
dc.description.abstractBackground and Aim Diabetic dyslipidaemia is common in type 2 diabetes (T2D) and insulin resistance and often precedes the onset of T2D. The Taq1B polymorphism in CETP (B1 and B2 alleles) (rs708272) and the G-250A polymorphism in LIPC (rs2070895) are associated with changes in enzyme activity and lipid concentrations. Our aim was to assess the effects of both polymorphisms on the risk of T2D. Methods and Results In a case-control study from the population-based Telde cohort, both polymorphisms were analysed by PCR-based methods. Subjects were classified, according to an oral glucose tolerance test, into diabetic (N = 115) and pre-diabetic (N = 116); 226 subjects with normal glucose tolerance, matched for age and gender, were included as controls. Chi-square (comparison between groups) and logistic regression (identification of independent effects) were used for analysis. The B1B1 Taq1B CETP genotype frequency increased with worsening glucose metabolism (42.5%, 46.1% and 54.3% in control, IGR and diabetic group; p = 0.042). This polymorphism was independently associated with an increased risk of diabetes (OR: 1.828; IC 95%: 1.12–2.99; p = 0.016), even after adjusting by confounding variables, whereas the LIPC polymorphism was not. Regarding the interaction between both polymorphisms, in the B1B1 genotype carriers, the absence of the minor (A) allele of the LIPC polymorphism increased the risk of having diabetes. Conclusion The presence of the B1B1 Taq1B CETP genotype contributes to the presence of diabetes, independently of age, sex, BMI and waist. However, among carriers of B1B1, the presence of GG genotype of the -250 LIPC polymorphism increases this risk further.en_US
dc.languageengen_US
dc.relation.ispartofPLoS ONEen_US
dc.sourcePLoS ONE [ISSN 1932-6203], v. 6 (11), (Noviembre 2011)en_US
dc.subject32 Ciencias médicasen_US
dc.subject.otherHigh-Density-Lipoproteinen_US
dc.subject.otherImpaired Glucose-Toleranceen_US
dc.subject.otherPlasma-Lipid Levelsen_US
dc.subject.otherCetp Geneen_US
dc.subject.otherPromoter Polymorphismen_US
dc.subject.otherTriglyceride Lipaseen_US
dc.subject.otherInsulin-Resistanceen_US
dc.subject.otherHeart-Diseaseen_US
dc.subject.otherFatty-Acidsen_US
dc.subject.otherAssociationen_US
dc.titleInteraction between Cholesteryl Ester Transfer Protein and Hepatic Lipase Encoding Genes and the Risk of Type 2 Diabetes: Results from the Telde Studyen_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1371/journal.pone.0027208en_US
dc.identifier.scopus2-s2.0-84875407187-
dc.identifier.scopus84875407187-
dc.identifier.isi000297197000032-
dc.contributor.authorscopusid33068166900-
dc.contributor.authorscopusid12786120600-
dc.contributor.authorscopusid6701324062-
dc.contributor.authorscopusid55130599700-
dc.contributor.authorscopusid21736048400-
dc.contributor.authorscopusid7401456520-
dc.identifier.eissn1932-6203-
dc.identifier.issuee27208-
dc.relation.volume6en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.contributor.daisngid1964185-
dc.contributor.daisngid556390-
dc.contributor.daisngid880609-
dc.contributor.daisngid6993936-
dc.contributor.daisngid10291807-
dc.contributor.daisngid450201-
dc.description.numberofpages7en_US
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Lopez-Rios, L-
dc.contributor.wosstandardWOS:Novoa, FJ-
dc.contributor.wosstandardWOS:Chirino, R-
dc.contributor.wosstandardWOS:Varillas, F-
dc.contributor.wosstandardWOS:Boronat-Cortes, M-
dc.contributor.wosstandardWOS:Wagner, AM-
dc.date.coverdateNoviembre 2011en_US
dc.identifier.ulpgces
dc.description.sjr2,369
dc.description.jcr4,092
dc.description.sjrqQ1
dc.description.jcrqQ1
dc.description.scieSCIE
dc.description.erihplusERIH PLUS
item.grantfulltextopen-
item.fulltextCon texto completo-
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.deptGIR IUIBS: Diabetes y endocrinología aplicada-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Médicas y Quirúrgicas-
crisitem.author.deptGIR IUIBS: Diabetes y endocrinología aplicada-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Médicas y Quirúrgicas-
crisitem.author.orcid0000-0002-5681-8931-
crisitem.author.orcid0000-0001-8535-8543-
crisitem.author.orcid0000-0002-7663-9308-
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.fullNameChirino Godoy, Ricardo-
crisitem.author.fullNameBoronat Cortés, Mauro-
crisitem.author.fullNameWägner, Anna Maria Claudia-
Colección:Artículos
miniatura
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