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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP-
dc.contributor.authorRODRIGUES, A. C.-
dc.contributor.authorSOBRINO, B.-
dc.contributor.authorGENVIGIR, F. D. V.-
dc.contributor.authorWILLRICH, M. A. V.-
dc.contributor.authorARAZI, S. S.-
dc.contributor.authorDOREA, E. L.-
dc.contributor.authorBERNIK, M. M. S.-
dc.contributor.authorBERTOLAMI, M.-
dc.contributor.authorFALUDI, A. A.-
dc.contributor.authorBRION, M. J.-
dc.contributor.authorCARRACEDO, A.-
dc.contributor.authorHIRATA, M. H.-
dc.contributor.authorHIRATA, R. D. C.-
dc.date.accessioned2013-09-23T16:59:04Z-
dc.date.available2013-09-23T16:59:04Z-
dc.date.issued2013-
dc.identifier.citationCLINICA CHIMICA ACTA, v.417, p.8-11, 2013-
dc.identifier.issn0009-8981-
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/2465-
dc.description.abstractObjective: Using candidate gene approach, we have investigated the effect of single nucleotide polymorphism (SNP) in genes related to lipid metabolism and atherosclerosis on dyslipidemia and atorvastatin response. Methods: The study included 157 patients treated with atorvastatin and 145 controls. Genomic DNA was isolated and genotyped using SNPlex technology. Results: Allele and genotype disease association test revealed that APOB rs693 (OR: 2.2 [1.5-3.2], p = 0.0001) and CD36 rs1984112 (OR: 3.7 [1.9-7.0], p = 0.0002) SNPs were independent risk factors for hypercholesterolemia. Only APOB rs693 T variant allele was associated with increased LDL cholesterol levels (> 160 mg/dL). After atorvastatin treatment (10 mg/day/4 weeks), LIPC - 514T allele was positively associated with LDL cholesterol reduction. Conclusion: The current study reinforces the current knowledge that carrying APOB rs693 is an independent risk factor for dyslipidemia and higher LDL levels. Furthermore, we found that a variant of CD36 was associated with dyslipidemia as a risk (rs1984112) factor. Finally, atorvastatin response could be predicted by LIPC - 514C>T SNP and physical activity. In conclusion, our data evidences the contribution of genetic markers and their interaction with environmental factor in the variability of statin response.-
dc.description.sponsorshipFAPESP [2008/06667-9]-
dc.description.sponsorshipFAPESP, Sao Paulo, Brazil-
dc.description.sponsorshipCNPq, Brasilia, Brazil-
dc.language.isoeng-
dc.publisherELSEVIER SCIENCE BV-
dc.relation.ispartofClinica Chimica Acta-
dc.rightsrestrictedAccess-
dc.subjectAssociation studies-
dc.subjectDyslipidemia-
dc.subjectSNPs-
dc.subjectStatins-
dc.subjectpharmacogenomics-
dc.subject.otherhepatic lipase gene-
dc.subject.otherdensity-lipoprotein cholesterol-
dc.subject.othergenome-wide association-
dc.subject.othercoronary-heart-disease-
dc.subject.othernonfasting triglycerides-
dc.subject.otherpromoter variant-
dc.subject.othercommon-
dc.subject.otherpolymorphism-
dc.subject.otherpopulation-
dc.subject.otherrisk-
dc.titleGenetic variants in genes related to lipid metabolism and atherosclerosis, dyslipidemia and atorvastatin response-
dc.typearticle-
dc.rights.holderCopyright ELSEVIER SCIENCE BV-
dc.identifier.doi10.1016/j.cca.2012.11.028-
dc.identifier.pmid23247049-
dc.subject.wosMedical Laboratory Technology-
dc.type.categoryoriginal article-
dc.type.versionpublishedVersion-
hcfmusp.author.externalRODRIGUES, A. C.:Univ Sao Paulo, Fac Ciencias Farmaceut, BR-09500900 Sao Paulo, Brazil-
hcfmusp.author.externalSOBRINO, B.:Fdn Publ Galega Med Xen, CIBERER, Grp Med Xen USC, Santiago De Compostela, Galicia, Spain-
hcfmusp.author.externalGENVIGIR, F. D. V.:Univ Sao Paulo, Fac Ciencias Farmaceut, BR-09500900 Sao Paulo, Brazil-
hcfmusp.author.externalWILLRICH, M. A. V.:Univ Sao Paulo, Fac Ciencias Farmaceut, BR-09500900 Sao Paulo, Brazil-
hcfmusp.author.externalARAZI, S. S.:Univ Sao Paulo, Fac Ciencias Farmaceut, BR-09500900 Sao Paulo, Brazil-
hcfmusp.author.externalBERTOLAMI, M.:Inst Dante Pazzanese Cardiol, Sao Paulo, Brazil-
hcfmusp.author.externalFALUDI, A. A.:Inst Dante Pazzanese Cardiol, Sao Paulo, Brazil-
hcfmusp.author.externalBRION, M. J.:Fdn Publ Galega Med Xen, CIBERER, Grp Med Xen USC, Santiago De Compostela, Galicia, Spain; Complexo Hosp Santiago de Compostela, Galicia, Spain-
hcfmusp.author.externalCARRACEDO, A.:Fdn Publ Galega Med Xen, CIBERER, Grp Med Xen USC, Santiago De Compostela, Galicia, Spain-
hcfmusp.author.externalHIRATA, M. H.:Univ Sao Paulo, Fac Ciencias Farmaceut, BR-09500900 Sao Paulo, Brazil-
hcfmusp.author.externalHIRATA, R. D. C.:Univ Sao Paulo, Fac Ciencias Farmaceut, BR-09500900 Sao Paulo, Brazil-
hcfmusp.description.beginpage8-
hcfmusp.description.endpage11-
hcfmusp.description.volume417-
hcfmusp.origemWOS-
hcfmusp.origem.idWOS:000315538700002-
hcfmusp.origem.id2-s2.0-84871750175-
hcfmusp.publisher.cityAMSTERDAM-
hcfmusp.publisher.countryNETHERLANDS-
hcfmusp.relation.referenceBansal S, 2007, JAMA-J AM MED ASSOC, V298, P309, DOI 10.1001/jama.298.3.309-
hcfmusp.relation.referenceBenn M, 2008, J CLIN ENDOCR METAB, V93, P1038, DOI 10.1210/jc.2007-1365-
hcfmusp.relation.referenceBerk-Planken IIL, 2003, DIABETES CARE, V26, P427, DOI 10.2337/diacare.26.2.427-
hcfmusp.relation.referenceBreslow JL, 2000, ANNU REV GENET, V34, P233, DOI 10.1146/annurev.genet.34.1.233-
hcfmusp.relation.referenceCenarro A, 2005, AM HEART J, V150, P1154, DOI 10.1016/j.ahj.2005.02.006-
hcfmusp.relation.referenceDeeb SS, 2000, J LIPID RES, V41, P155-
hcfmusp.relation.referenceEdwards Jayne E, 2003, BMC Fam Pract, V4, P18, DOI 10.1186/1471-2296-4-18-
hcfmusp.relation.referenceGotto AM, 2004, J AM COLL CARDIOL, V43, P717, DOI 10.1016/j.jacc.2003.08.061-
hcfmusp.relation.referenceGrundy SM, 2004, CIRCULATION, V110, P227, DOI 10.1161/01.CIR.0000133317.49796.0E-
hcfmusp.relation.referenceKathiresan S, 2007, BMC MED GENET, V8, DOI 10.1186/1471-2350-8-S1-S17-
hcfmusp.relation.referenceLepretre F, 2004, ATHEROSCLEROSIS, V173, P375, DOI 10.1016/j.atherosclerosis.2003.12.029-
hcfmusp.relation.referenceLove-Gregory L, 2008, HUM MOL GENET, V17, P1695, DOI 10.1093/hmg/ddn060-
hcfmusp.relation.referenceMaggo SDS, 2011, DRUG SAFETY, V34, P1, DOI 10.2165/11584380-000000000-00000-
hcfmusp.relation.referenceMangravite LM, 2008, CURR OPIN MOL THER, V10, P555-
hcfmusp.relation.referenceMorcillo-Suarez C, 2008, BIOINFORMATICS, V24, P2790-
hcfmusp.relation.referenceNordestgaard BG, 2007, JAMA-J AM MED ASSOC, V298, P299, DOI 10.1001/jama.298.3.299-
hcfmusp.relation.referencePilia G, 2006, PLOS GENET, V2, P1207, DOI 10.1371/journal.pgen.0020132-
hcfmusp.relation.referencePollin TI, 2004, ATHEROSCLEROSIS, V173, P89, DOI 10.1016/j.atherosclerosis.2003.11.012-
hcfmusp.relation.referenceRodrigues AC, 2007, CURR OPIN MOL THER, V9, P545-
hcfmusp.relation.referenceRodrigues AC, 2011, INT J MOL SCI, V12, P5815, DOI 10.3390/ijms12095815-
hcfmusp.relation.referenceSandhu MS, 2008, LANCET, V371, P483, DOI 10.1016/S0140-6736(08)60208-1-
hcfmusp.relation.referenceTeslovich TM, 2010, NATURE, V466, P707, DOI 10.1038/nature09270-
hcfmusp.relation.referenceZambon A, 1998, ARTERIOSCL THROM VAS, V18, P1723-
hcfmusp.relation.referenceZambon A, 2001, CIRCULATION, V103, P792-
hcfmusp.relation.referenceZhu H, 2007, HUM MOL GENET, V16, P1765, DOI 10.1093/hmg/ddm124-
dc.description.indexMEDLINE-
hcfmusp.remissive.sponsorshipCNPq-
hcfmusp.remissive.sponsorshipFAPESP-
hcfmusp.citation.scopus26-
hcfmusp.scopus.lastupdate2022-05-06-
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