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http://purl.uniprot.org/citations/29441581http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29441581http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Single nucleotide polymorphisms in serotonin 2C receptor (HTR2C), leptin (LEP), and leptin receptor (LEPR) genes are reportedly associated with the presence of metabolic syndrome (MS). We investigated whether HTR2C:rs518147 (-697G/C), rs12836771 (A/G), LEP: rs7799039 (-2548G/A) and LEPR:rs1137101 (668A/G) are related to MS in psychotic disorder patients treated with atypical antipsychotics.

Methods

A cross-sectional study including 200 patients was conducted; genetic polymorphisms in HTR2C (rs518147 and rs12836771), LEP (rs7799039) and LEPR (rs1137101) were genotyped. The presence of MS was evaluated according to the 2005 International Diabetes Federation (IDF) Asia criteria. The associations of genetic factors with the presence of MS are analysed.

Key findings

Two SNPs in the HTR2C gene but not LEP and LEPR were associated with the presence of MS after adjustment for the combination of atypical antipsychotics. With respect to the effect of gender after treatment with risperidone and clozapine was statistically significant. Moreover, genotype combinations had no effect on MS.

Conclusions

Therefore, HTR2C genetic variants may be involved in the susceptibility to MS in patients treated with atypical antipsychotics. Additionally, there was a gender effect in the presence of MS. No effect of LEP or LEPR polymorphisms or the combination of HTR2C-LEP and HTR2C-LEPR was observed for the presence of MS."xsd:string
http://purl.uniprot.org/citations/29441581http://purl.org/dc/terms/identifier"doi:10.1111/jphp.12892"xsd:string
http://purl.uniprot.org/citations/29441581http://purl.uniprot.org/core/author"Sukasem C."xsd:string
http://purl.uniprot.org/citations/29441581http://purl.uniprot.org/core/author"Koomdee N."xsd:string
http://purl.uniprot.org/citations/29441581http://purl.uniprot.org/core/author"Puangpetch A."xsd:string
http://purl.uniprot.org/citations/29441581http://purl.uniprot.org/core/author"Jiratjintana N."xsd:string
http://purl.uniprot.org/citations/29441581http://purl.uniprot.org/core/author"Unaharassamee W."xsd:string
http://purl.uniprot.org/citations/29441581http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/29441581http://purl.uniprot.org/core/name"J Pharm Pharmacol"xsd:string
http://purl.uniprot.org/citations/29441581http://purl.uniprot.org/core/pages"536-542"xsd:string
http://purl.uniprot.org/citations/29441581http://purl.uniprot.org/core/title"Genetic polymorphisms of HTR2C, LEP and LEPR on metabolic syndromes in patients treated with atypical antipsychotic drugs."xsd:string
http://purl.uniprot.org/citations/29441581http://purl.uniprot.org/core/volume"70"xsd:string
http://purl.uniprot.org/citations/29441581http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/29441581
http://purl.uniprot.org/citations/29441581http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/29441581
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http://purl.uniprot.org/uniprot/P28335http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/29441581
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