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. 2021 Mar 5;11(3):181.
doi: 10.3390/jpm11030181.

Genetic Polymorphisms of 5-HT Receptors and Antipsychotic-Induced Metabolic Dysfunction in Patients with Schizophrenia

Diana Z Paderina  1 , Anastasiia S Boiko  1 , Ivan V Pozhidaev  1 , Anna V Bocharova  2 , Irina A Mednova  1 , Olga Yu Fedorenko  1 , Elena G Kornetova  1   3 , Anton J M Loonen  4 , Arkadiy V Semke  1 , Nikolay A Bokhan  1   3 , Svetlana A Ivanova  1   3
Affiliations

Genetic Polymorphisms of 5-HT Receptors and Antipsychotic-Induced Metabolic Dysfunction in Patients with Schizophrenia

Diana Z Paderina et al. J Pers Med. .

Abstract

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.

Keywords: antipsychotics; body mass index; genes; metabolic syndrome; pharmacogenetics; schizophrenia; serotonin; weight gain.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

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References

    1. De Hert M., Detraux J., van Winkel R., Yu W., Correll C.U. Metabolic and cardiovascular adverse effects associated with antipsychotic drugs. Nat. Rev. Endocrinol. 2011;8:114–126. doi: 10.1038/nrendo.2011.156. - DOI - PubMed
    1. O’Neill S., O’Driscoll L. Metabolic syndrome: A closer look at the growing epidemic and its associated pathologies. Obes. Rev. 2015;16:1–12. doi: 10.1111/obr.12229. - DOI - PubMed
    1. Rojo L.E., Gaspar P.A., Silva H., Risco L., Arena P., Cubillos-Robles K., Jara B. Metabolic syndrome and obesity among users of second generation antipsychotics: A global challenge for modern psychopharmacology. Pharmacol. Res. 2015;101:74–85. doi: 10.1016/j.phrs.2015.07.022. - DOI - PubMed
    1. Freyberg Z., Aslanoglou D., Shah R., Ballon J.S. Intrinsic and Antipsychotic Drug-Induced Metabolic Dysfunction in Schizophrenia. Front. Neurosci. 2017;11:432. doi: 10.3389/fnins.2017.00432. - DOI - PMC - PubMed
    1. Ijaz S., Bolea B., Davies S., Savović J., Richards A., Sullivan S., Moran P. Antipsychotic polypharmacy and metabolic syndrome in schizophrenia: A review of systematic reviews. BMC Psychiatry. 2018;18:275. doi: 10.1186/s12888-018-1848-y. - DOI - PMC - PubMed

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