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Vitamin D deficiency in gestational diabetes mellitus and the role of the placenta

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dc.contributor.authorCho, Geum Joon-
dc.contributor.authorHong, Soon-Cheol-
dc.contributor.authorOh, Min-Jeong-
dc.contributor.authorKim, Hai-Joong-
dc.date.accessioned2021-09-05T18:09:12Z-
dc.date.available2021-09-05T18:09:12Z-
dc.date.created2021-06-15-
dc.date.issued2013-12-
dc.identifier.issn0002-9378-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/101346-
dc.description.abstractOBJECTIVE: The aim of this study was to evaluate the relationships between maternal vitamin D levels and gestational diabetes mellitus (GDM) and differences in the placental production of vitamin D receptor (VDR), CYP24A, and CYP27B1. STUDY DESIGN: Forty normal pregnant women and 20 women with GDM were included in this study. Serum levels of 25-hydroxyvitamin D (25[OH]D) were measured with enzyme-linked immunosorbent assay. The expression and production of VDR, CYP27B1, and CYP24A1 in the placenta were evaluated with real time-polymerase chain reaction and Western blot, respectively. RESULTS: We found that 27.5% of normal pregnant women and 85% of women with GDM had vitamin D deficiency, with serum 25(OH)D levels <20 ng/mL. Serum levels of 25(OH)D were lower in women with GDM than normal pregnant women (P < .01). The production of CYP24A1 protein and messenger RNA expression was significantly higher in placental tissue from patients with GDM than in those from normal pregnancies; however, the production of CYP27B1 and VDR protein and messenger RNA expression were not different between 2 the groups. CONCLUSION: In this study, vitamin D deficiency was associated with GDM. Given that 25(OH)D is hydroxylated by CYP27B1 to the bioactive 1,25(OH)(2)D form, and CYP24A1 catabolizes both 25(OH)D and 1,25(OH)(2)D to the inactive metabolites, respectively, our data indicate that the elevated activity of CYP24A1 in the placenta may play a key role in the development of vitamin D deficiency in GDM.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherMOSBY-ELSEVIER-
dc.subjectINSULIN-RESISTANCE-
dc.subjectMESSENGER-RNA-
dc.subjectCALCIUM HOMEOSTASIS-
dc.subjectHUMAN-PREGNANCY-
dc.subjectLACTATION-
dc.subjectCELLS-
dc.subjectRISK-
dc.subjectINFLAMMATION-
dc.subjectMETABOLISM-
dc.subjectSECRETION-
dc.titleVitamin D deficiency in gestational diabetes mellitus and the role of the placenta-
dc.typeArticle-
dc.contributor.affiliatedAuthorCho, Geum Joon-
dc.contributor.affiliatedAuthorHong, Soon-Cheol-
dc.contributor.affiliatedAuthorOh, Min-Jeong-
dc.contributor.affiliatedAuthorKim, Hai-Joong-
dc.identifier.doi10.1016/j.ajog.2013.08.015-
dc.identifier.scopusid2-s2.0-84888580924-
dc.identifier.wosid000327538900017-
dc.identifier.bibliographicCitationAMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, v.209, no.6-
dc.relation.isPartOfAMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY-
dc.citation.titleAMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY-
dc.citation.volume209-
dc.citation.number6-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaObstetrics & Gynecology-
dc.relation.journalWebOfScienceCategoryObstetrics & Gynecology-
dc.subject.keywordPlusINSULIN-RESISTANCE-
dc.subject.keywordPlusMESSENGER-RNA-
dc.subject.keywordPlusCALCIUM HOMEOSTASIS-
dc.subject.keywordPlusHUMAN-PREGNANCY-
dc.subject.keywordPlusLACTATION-
dc.subject.keywordPlusCELLS-
dc.subject.keywordPlusRISK-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusMETABOLISM-
dc.subject.keywordPlusSECRETION-
dc.subject.keywordAuthorgestational diabetes mellitus-
dc.subject.keywordAuthorplacenta-
dc.subject.keywordAuthorvitamin D-
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