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Haplotype combination of Calpain-10 gene polymorphism is associated with metabolic syndrome in type 2 diabetes

DC Field Value Language
dc.contributor.author강은석-
dc.contributor.author명성민-
dc.contributor.author안철우-
dc.contributor.author이유미-
dc.contributor.author이현철-
dc.contributor.author차봉수-
dc.date.accessioned2015-06-10T12:25:43Z-
dc.date.available2015-06-10T12:25:43Z-
dc.date.issued2006-
dc.identifier.issn0168-8227-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/109783-
dc.description.abstractPatients with metabolic syndrome are at increased risk of developing cardiovascular disease. The combinations of the haplotype created by the alleles of three single nucleotide polymorphisms (SNPs): SNP-43, -19, and -63 of the Calpain-10 gene (CAPN10), have been reported to be associated with the risk of type 2 diabetes in many populations. The aim of this study was to examine the association of the CAPN10 polymorphism with metabolic syndrome in patients with type 2 diabetes in Korea. Overall, 382 patients with type 2 diabetes were enrolled in this study. All the subjects were genotyped according to CAPN10 SNP-43, -19, and -63. The restriction fragment length polymorphism method was used for the three SNPs. The baseline presence of components of metabolic syndrome was determined. Two hundred and sixty-five (69.4%) patients had metabolic syndrome. Patients with the 111/121 haplotype combination showed a higher risk of hypertension than the other haplotype combinations (odd ratio (OR) = 2.334, P = 0.010). Patients with the 111/121 haplotype combination had a significantly high risk of metabolic syndrome (OR = 1.927, P = 0.042). The results of this study suggest that a novel 111/121 haplotype combination created by the CAPN10 SNP-43, -19, and -63 increases the susceptibility to the metabolic syndrome in patients with type 2 diabetes.-
dc.description.statementOfResponsibilityopen-
dc.format.extent268~275-
dc.relation.isPartOfDIABETES RESEARCH AND CLINICAL PRACTICE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdult-
dc.subject.MESHBlood Glucose/analysis-
dc.subject.MESHBlood Pressure/physiology-
dc.subject.MESHCalpain/genetics*-
dc.subject.MESHCholesterol, HDL/blood-
dc.subject.MESHDiabetes Mellitus, Type 2/blood-
dc.subject.MESHDiabetes Mellitus, Type 2/genetics*-
dc.subject.MESHDiabetes Mellitus, Type 2/physiopathology-
dc.subject.MESHFemale-
dc.subject.MESHGene Frequency-
dc.subject.MESHGenetic Predisposition to Disease/genetics-
dc.subject.MESHGenotype-
dc.subject.MESHGlycated Hemoglobin A/metabolism-
dc.subject.MESHHaplotypes/genetics*-
dc.subject.MESHHumans-
dc.subject.MESHKorea-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHOdds Ratio-
dc.subject.MESHPolymorphism, Single Nucleotide/genetics*-
dc.subject.MESHTriglycerides/blood-
dc.titleHaplotype combination of Calpain-10 gene polymorphism is associated with metabolic syndrome in type 2 diabetes-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorEun Seok Kang-
dc.contributor.googleauthorMoonsuk Nam-
dc.contributor.googleauthorHye Joo Kim-
dc.contributor.googleauthorHyeong Jin Kim-
dc.contributor.googleauthorSung Min Myoung-
dc.contributor.googleauthorYumie Rhee-
dc.contributor.googleauthorChul Woo Ahn-
dc.contributor.googleauthorBong Soo Cha-
dc.contributor.googleauthorHyun Chul Lee-
dc.identifier.doi10.1016/j.diabres.2006.01.011-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00068-
dc.contributor.localIdA01350-
dc.contributor.localIdA02270-
dc.contributor.localIdA03012-
dc.contributor.localIdA03301-
dc.contributor.localIdA03996-
dc.relation.journalcodeJ00723-
dc.identifier.eissn1872-8227-
dc.identifier.pmid16546286-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0168822706000386-
dc.subject.keywordCalpain-10-
dc.subject.keywordPolymorphism-
dc.subject.keywordHaplotype-
dc.subject.keywordMetabolic syndrome-
dc.contributor.alternativeNameKang, Eun Seok-
dc.contributor.alternativeNameMyung, Sung Min-
dc.contributor.alternativeNameAhn, Chul Woo-
dc.contributor.alternativeNameRhee, Yumie-
dc.contributor.alternativeNameLee, Hyun Chul-
dc.contributor.alternativeNameCha, Bong Soo-
dc.contributor.affiliatedAuthorKang, Eun Seok-
dc.contributor.affiliatedAuthorMyung, Sung Min-
dc.contributor.affiliatedAuthorAhn, Chul Woo-
dc.contributor.affiliatedAuthorRhee, Yumie-
dc.contributor.affiliatedAuthorLee, Hyun Chul-
dc.contributor.affiliatedAuthorCha, Bong Soo-
dc.rights.accessRightsnot free-
dc.citation.volume73-
dc.citation.number3-
dc.citation.startPage268-
dc.citation.endPage275-
dc.identifier.bibliographicCitationDIABETES RESEARCH AND CLINICAL PRACTICE, Vol.73(3) : 268-275, 2006-
dc.identifier.rimsid53418-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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