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Cannabinoid type 1 receptor gene polymorphisms are not associated with olanzapine-induced weight gain

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dc.contributor.authorPark, Young-Min-
dc.contributor.authorChoi, Jung-Eun-
dc.contributor.authorKang, Seung-Gul-
dc.contributor.authorKoo, Seung-Hoi-
dc.contributor.authorKim, Leen-
dc.contributor.authorGeum, Dongho-
dc.contributor.authorLee, Heon-Jeong-
dc.date.available2020-11-03T03:44:28Z-
dc.date.issued2011-06-
dc.identifier.issn0885-6222-
dc.identifier.issn1099-1077-
dc.identifier.urihttps://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/13433-
dc.description.abstractBackground Olanzapine is an atypical antipsychotic known to cause considerable weight gain. The cannabinoid type 1 receptor has been reported to be involved in energy balance control, appetite stimulation, and increases in body weight. Methods In the present study, we investigated three polymorphisms (rs1049353, rs806368, and rs4707436) in the cannabinoid type 1 receptor gene (CNR1) and weight gain in Korean patients with schizophrenia receiving olanzapine treatment. Weight and height were measured prior to starting olanzapine and again after long-term treatment in 78 patients with schizophrenia. CNR1 polymorphisms were genotyped using PCR-RFLP methods. Results The three CNR1 polymorphisms were not associated with body weight changes from baseline to the endpoint after olanzapine treatment (p > 0.05). There were also no significant differences in genotype, allele, or haplotype frequencies between the high weight gain (at least 7%) and low weight gain (less than 7%) groups. Conclusion Within the limitations imposed by the smallness of the clinical sample, our findings suggest that CNR1 polymorphisms are not associated with olanzapine-induced weight gain. Copyright (C) 2011 John Wiley & Sons, Ltd.-
dc.format.extent6-
dc.language영어-
dc.language.isoENG-
dc.publisherWILEY-
dc.titleCannabinoid type 1 receptor gene polymorphisms are not associated with olanzapine-induced weight gain-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1002/hup.1210-
dc.identifier.scopusid2-s2.0-79960835205-
dc.identifier.wosid000293964700008-
dc.identifier.bibliographicCitationHUMAN PSYCHOPHARMACOLOGY-CLINICAL AND EXPERIMENTAL, v.26, no.4-5, pp 332 - 337-
dc.citation.titleHUMAN PSYCHOPHARMACOLOGY-CLINICAL AND EXPERIMENTAL-
dc.citation.volume26-
dc.citation.number4-5-
dc.citation.startPage332-
dc.citation.endPage337-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalResearchAreaPsychiatry-
dc.relation.journalResearchAreaPsychology-
dc.relation.journalWebOfScienceCategoryClinical Neurology-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryPsychiatry-
dc.relation.journalWebOfScienceCategoryPsychology-
dc.subject.keywordPlusBODY-MASS INDEX-
dc.subject.keywordPlusQUALITY-OF-LIFE-
dc.subject.keywordPlusATYPICAL ANTIPSYCHOTICS-
dc.subject.keywordPlusENDOCANNABINOID SYSTEM-
dc.subject.keywordPlusNO EVIDENCE-
dc.subject.keywordPlusCNR1-
dc.subject.keywordPlusOBESITY-
dc.subject.keywordPlusPHARMACOLOGY-
dc.subject.keywordPlusADHERENCE-
dc.subject.keywordPlusRISK-
dc.subject.keywordAuthorolanzapine-
dc.subject.keywordAuthorcannabinoid receptor-
dc.subject.keywordAuthorweight gain-
dc.subject.keywordAuthorpolymorphism-
dc.subject.keywordAuthorschizophrenia-
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