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Genetic Polymorphisms of 5-HT Receptors and Antipsychotic-Induced Metabolic Dysfunction in Patients with Schizophrenia
Background: Antipsychotic-induced metabolic syndrome (MetS) is a multifactorial disease with a genetic predisposition. Serotonin and its receptors are involved in antipsychotic-drug-induced metabolic disorders. The present study investigated the association of nine polymorphisms in the four 5-hydrox...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7999828/ https://www.ncbi.nlm.nih.gov/pubmed/33807811 http://dx.doi.org/10.3390/jpm11030181 |
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author | Paderina, Diana Z. Boiko, Anastasiia S. Pozhidaev, Ivan V. Bocharova, Anna V. Mednova, Irina A. Fedorenko, Olga Yu. Kornetova, Elena G. Loonen, Anton J.M. Semke, Arkadiy V. Bokhan, Nikolay A. Ivanova, Svetlana A. |
author_facet | Paderina, Diana Z. Boiko, Anastasiia S. Pozhidaev, Ivan V. Bocharova, Anna V. Mednova, Irina A. Fedorenko, Olga Yu. Kornetova, Elena G. Loonen, Anton J.M. Semke, Arkadiy V. Bokhan, Nikolay A. Ivanova, Svetlana A. |
author_sort | Paderina, Diana Z. |
collection | PubMed |
description | Background: Antipsychotic-induced metabolic syndrome (MetS) is a multifactorial disease with a genetic predisposition. Serotonin and its receptors are involved in antipsychotic-drug-induced metabolic disorders. The present study investigated the association of nine polymorphisms in the four 5-hydroxytryptamine receptor (HTR) genes HTR1A, HTR2A, HTR3A, and HTR2C and the gene encoding for the serotonin transporter SLC6A4 with MetS in patients with schizophrenia. Methods: A set of nine single-nucleotide polymorphisms of genes of the serotonergic system was investigated in a population of 475 patients from several Siberian regions (Russia) with a clinical diagnosis of schizophrenia. Genotyping was performed and the results were analyzed using chi-square tests. Results: Polymorphic variant rs521018 (HTR2C) was associated with higher body mass index in patients receiving long-term antipsychotic therapy, but not with drug-induced metabolic syndrome. Rs1150226 (HTR3A) was also associated but did not meet Hardy–Weinberg equilibrium. Conclusions: Our results indicate that allelic variants of HTR2C genes may have consequences on metabolic parameters. MetS may have too complex a mechanistic background to be studied without dissecting the syndrome into its individual (causal) components. |
format | Online Article Text |
id | pubmed-7999828 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-79998282021-03-28 Genetic Polymorphisms of 5-HT Receptors and Antipsychotic-Induced Metabolic Dysfunction in Patients with Schizophrenia Paderina, Diana Z. Boiko, Anastasiia S. Pozhidaev, Ivan V. Bocharova, Anna V. Mednova, Irina A. Fedorenko, Olga Yu. Kornetova, Elena G. Loonen, Anton J.M. Semke, Arkadiy V. Bokhan, Nikolay A. Ivanova, Svetlana A. J Pers Med Communication Background: Antipsychotic-induced metabolic syndrome (MetS) is a multifactorial disease with a genetic predisposition. Serotonin and its receptors are involved in antipsychotic-drug-induced metabolic disorders. The present study investigated the association of nine polymorphisms in the four 5-hydroxytryptamine receptor (HTR) genes HTR1A, HTR2A, HTR3A, and HTR2C and the gene encoding for the serotonin transporter SLC6A4 with MetS in patients with schizophrenia. Methods: A set of nine single-nucleotide polymorphisms of genes of the serotonergic system was investigated in a population of 475 patients from several Siberian regions (Russia) with a clinical diagnosis of schizophrenia. Genotyping was performed and the results were analyzed using chi-square tests. Results: Polymorphic variant rs521018 (HTR2C) was associated with higher body mass index in patients receiving long-term antipsychotic therapy, but not with drug-induced metabolic syndrome. Rs1150226 (HTR3A) was also associated but did not meet Hardy–Weinberg equilibrium. Conclusions: Our results indicate that allelic variants of HTR2C genes may have consequences on metabolic parameters. MetS may have too complex a mechanistic background to be studied without dissecting the syndrome into its individual (causal) components. MDPI 2021-03-05 /pmc/articles/PMC7999828/ /pubmed/33807811 http://dx.doi.org/10.3390/jpm11030181 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ). |
spellingShingle | Communication Paderina, Diana Z. Boiko, Anastasiia S. Pozhidaev, Ivan V. Bocharova, Anna V. Mednova, Irina A. Fedorenko, Olga Yu. Kornetova, Elena G. Loonen, Anton J.M. Semke, Arkadiy V. Bokhan, Nikolay A. Ivanova, Svetlana A. Genetic Polymorphisms of 5-HT Receptors and Antipsychotic-Induced Metabolic Dysfunction in Patients with Schizophrenia |
title | Genetic Polymorphisms of 5-HT Receptors and Antipsychotic-Induced Metabolic Dysfunction in Patients with Schizophrenia |
title_full | Genetic Polymorphisms of 5-HT Receptors and Antipsychotic-Induced Metabolic Dysfunction in Patients with Schizophrenia |
title_fullStr | Genetic Polymorphisms of 5-HT Receptors and Antipsychotic-Induced Metabolic Dysfunction in Patients with Schizophrenia |
title_full_unstemmed | Genetic Polymorphisms of 5-HT Receptors and Antipsychotic-Induced Metabolic Dysfunction in Patients with Schizophrenia |
title_short | Genetic Polymorphisms of 5-HT Receptors and Antipsychotic-Induced Metabolic Dysfunction in Patients with Schizophrenia |
title_sort | genetic polymorphisms of 5-ht receptors and antipsychotic-induced metabolic dysfunction in patients with schizophrenia |
topic | Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7999828/ https://www.ncbi.nlm.nih.gov/pubmed/33807811 http://dx.doi.org/10.3390/jpm11030181 |
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