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Possible association between the-2548A/G polymorphism of the leptin gene and olanzapine-induced weight gain

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dc.contributor.authorKang, Seung-Gul-
dc.contributor.authorLee, Heon-Jeong-
dc.contributor.authorPark, Young-Min-
dc.contributor.authorChoi, Jung-Eun-
dc.contributor.authorHan, Changsu-
dc.contributor.authorKim, Yong-Ku-
dc.contributor.authorKim, Seung-Hyun-
dc.contributor.authorLee, Min-Soo-
dc.contributor.authorJoe, Sook-Haeng-
dc.contributor.authorJung, In-Kwa-
dc.contributor.authorKim, Leen-
dc.date.available2020-11-03T10:48:33Z-
dc.date.issued2008-01-01-
dc.identifier.issn0278-5846-
dc.identifier.issn1878-4216-
dc.identifier.urihttps://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/17201-
dc.description.abstractAntipsychotic-induced weight gain has important effects on treatment compliance and long-term health. Several reports have indicated that a -2548A/G single-nucleotide polymorphism (SNP) of the leptin gene is associated with antipsychotic-induced weight gain. We hypothesized that there is a similar relationship between the -2548A/G SNP and olanzapine-induced weight gain. A total of 74 Korean schizophrenic patients were examined. Their weight was measured before starting olanzapine and after long-term treatment lasting for at least 3 months. The weight gain was significantly higher for patients with the AG genotype than for those with the AA genotype (p=0.029). Analysis of covariance also showed the difference of weight gain was still significant when adjusted for sex and treatment duration (p=0.046). This finding supports the presence of a relationship between the -2548A/G SNP of the leptin gene and weight gain in Korean schizophrenic patients receiving olanzapine treatment. (c) 2007 Elsevier Inc. All rights reserved.-
dc.format.extent4-
dc.language영어-
dc.language.isoENG-
dc.publisherPERGAMON-ELSEVIER SCIENCE LTD-
dc.titlePossible association between the-2548A/G polymorphism of the leptin gene and olanzapine-induced weight gain-
dc.typeArticle-
dc.publisher.location영국-
dc.identifier.doi10.1016/j.pnpbp.2007.08.002-
dc.identifier.scopusid2-s2.0-38349056887-
dc.identifier.wosid000253565500024-
dc.identifier.bibliographicCitationPROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY, v.32, no.1, pp 160 - 163-
dc.citation.titlePROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY-
dc.citation.volume32-
dc.citation.number1-
dc.citation.startPage160-
dc.citation.endPage163-
dc.type.docTypeReview-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalResearchAreaPsychiatry-
dc.relation.journalWebOfScienceCategoryClinical Neurology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryPsychiatry-
dc.subject.keywordPlusBODY-WEIGHT-
dc.subject.keywordPlusOBESE GENE-
dc.subject.keywordPlusOB PROTEIN-
dc.subject.keywordPlusCLOZAPINE-
dc.subject.keywordPlusREGION-
dc.subject.keywordPlusSCHIZOPHRENIA-
dc.subject.keywordPlusADIPOSITY-
dc.subject.keywordPlusMOUSE-
dc.subject.keywordAuthorleptin gene-
dc.subject.keywordAuthorolanzapine-
dc.subject.keywordAuthorpolymorphism-
dc.subject.keywordAuthorschizophrenia-
dc.subject.keywordAuthorweight gain-
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