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제2형 당뇨병환자에서의 인슐린양 성장인자 결합단백질-3(IGFBP-3) promoter -202 A/C 유전자 다형성

DC FieldValueLanguage
dc.contributor.author강은석-
dc.contributor.author김경래-
dc.contributor.author안철우-
dc.contributor.author이은직-
dc.contributor.author이현철-
dc.contributor.author임승길-
dc.contributor.author차봉수-
dc.date.accessioned2015-06-10T12:22:09Z-
dc.date.available2015-06-10T12:22:09Z-
dc.date.issued2006-
dc.identifier.issn1229-9693-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/109674-
dc.description.abstractBackgrounds: IGFs share approximately 50 percent of their amino acid with insulin and are largely bound to IGFBP-3, and they are known to be important in glucose metabolism. We evaluated the impact of IGFBP-3 promoter-202 polymorphism on concentration of IGF-I and IGFBP-3, and its relationship with different clinical characteristics of type 2 diabetes (T2DM). Method: A single nucleotide polymorphism at -202 locus of the IGFBP-3 promoter was genotyped for T2DM patients and the controls in their forties. Then, we compared concentrations of IGF-I and IGFBP-3, IGFBP-3 promoter-202 polymorphisms, and other clinical characteristics between diabetes group and the control. Results: Total of 169 subjects were enrolled. IGF-I levels of diabetes group were lower than those of the control, while IGFBP-3 levels of diabetes group were higher than the control. Among IGFBP-3 promoter -202 polymorphisms, AA occurred in 31 subjects (42.5%), AC in 33 (45.2%), and CC in 20 (27.4%) in control group. IGFBP-3 level was highest in AA group and lowest in CC group, and, IGF-I/IGFBP-3 molar ratio was lower in AA group than AC and CC groups. In diabetes group, AA occurred in 42 patients (50%) and AC in 42 patients (50%) without any significant difference between the two groups. IGF-I was in a negative correlation with weight, height, BMI and FBS. And IGFBP-3 correlated positively with BMI, FBS, and cholesterol. Conclusion: T2DM patients had decreased levels of IGF-I and increased levels of IGFBP-3, which can reduce IGF-I/IGFBP-3 molar ratio and free IGF-I. In other words, low free IGF-I level can give rise to T2DM. IGFBP-3 promoter -202 genotype has a control over concentration of IGFBP-3, but not weight, height, and BMI. However, IGFBP-3 is in a positive correlation with BMI. Thus, we propose that IGFBP-3 promoter -202 genotype may influence glucose metabolism not only by directly controlling IGFBP-3 concentration, but also through BMI indirectly.-
dc.description.statementOfResponsibilityopen-
dc.format.extent169~180-
dc.relation.isPartOfClinical Diabetes (임상당뇨병)-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.title제2형 당뇨병환자에서의 인슐린양 성장인자 결합단백질-3(IGFBP-3) promoter -202 A/C 유전자 다형성-
dc.title.alternativeGenetic Polymorphism of Insulin-like Growth Factor Binding Proein-3(IGBP-3) Promoter Gene in Type 2 DM patients-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthor남지선-
dc.contributor.googleauthor공지현-
dc.contributor.googleauthor노태웅-
dc.contributor.googleauthor김철식-
dc.contributor.googleauthor박종숙-
dc.contributor.googleauthor김혜진-
dc.contributor.googleauthor최유경-
dc.contributor.googleauthor임재윤-
dc.contributor.googleauthor강은석-
dc.contributor.googleauthor안철우-
dc.contributor.googleauthor차봉수-
dc.contributor.googleauthor이은직-
dc.contributor.googleauthor임승길-
dc.contributor.googleauthor김경래-
dc.contributor.googleauthor이현철-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00068-
dc.contributor.localIdA00294-
dc.contributor.localIdA02270-
dc.contributor.localIdA03050-
dc.contributor.localIdA03301-
dc.contributor.localIdA03375-
dc.contributor.localIdA03996-
dc.relation.journalcodeJ00568-
dc.subject.keywordInsulin-like growth factor-
dc.subject.keywordInsulin-like growth factor binding protein-3-
dc.subject.keywordInsulin-like growth factor binding protein-3 promoter -202 polymorphism-
dc.subject.keywordType 2 diabetes mellitus-
dc.contributor.alternativeNameKang, Eun Seok-
dc.contributor.alternativeNameKim, Kyung Rae-
dc.contributor.alternativeNameAhn, Chul Woo-
dc.contributor.alternativeNameLee, Eun Jig-
dc.contributor.alternativeNameLee, Hyun Chul-
dc.contributor.alternativeNameLim, Sung Kil-
dc.contributor.alternativeNameCha, Bong Soo-
dc.contributor.affiliatedAuthorKang, Eun Seok-
dc.contributor.affiliatedAuthorKim, Kyung Rae-
dc.contributor.affiliatedAuthorAhn, Chul Woo-
dc.contributor.affiliatedAuthorLee, Eun Jig-
dc.contributor.affiliatedAuthorLee, Hyun Chul-
dc.contributor.affiliatedAuthorLim, Sung Kil-
dc.contributor.affiliatedAuthorCha, Bong Soo-
dc.rights.accessRightsfree-
dc.citation.volume7-
dc.citation.number2-
dc.citation.startPage169-
dc.citation.endPage180-
dc.identifier.bibliographicCitationClinical Diabetes (임상당뇨병), Vol.7(2) : 169-180, 2006-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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