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dc.contributor.authorCarli, Marco
dc.contributor.authorKolachalam, Shivakumar
dc.contributor.authorLongoni, Biancamaria
dc.contributor.authorPintaudi, Anna
dc.contributor.authorBaldini, Marco
dc.contributor.authorAringhieri, Stefano
dc.contributor.authorFasciani, Irene
dc.contributor.authorAnnibale, Paolo
dc.contributor.authorMaggio, Roberto
dc.contributor.authorScarselli, Marco
dc.date.accessioned2022-01-12T17:30:03Z
dc.date.available2022-01-12T17:30:03Z
dc.date.issued2021-03-08
dc.identifier.citationCarli , M , Kolachalam , S , Longoni , B , Pintaudi , A , Baldini , M , Aringhieri , S , Fasciani , I , Annibale , P , Maggio , R & Scarselli , M 2021 , ' Atypical antipsychotics and metabolic syndrome : from molecular mechanisms to clinical differences ' , Pharmaceuticals , vol. 14 , no. 3 , 238 . https://doi.org/10.3390/ph14030238en
dc.identifier.issn1424-8247
dc.identifier.otherPURE: 277434085
dc.identifier.otherPURE UUID: a6113c98-ed62-4ba0-9157-d9eebba6effb
dc.identifier.otherScopus: 85103035093
dc.identifier.urihttp://hdl.handle.net/10023/24652
dc.description.abstractAtypical antipsychotics (AAPs) are commonly prescribed medications to treat schizophre-nia, bipolar disorders and other psychotic disorders. However, they might cause metabolic syndrome (MetS) in terms of weight gain, dyslipidemia, type 2 diabetes (T2D), and high blood pressure, which are responsible for reduced life expectancy and poor adherence. Importantly, there is clear evidence that early metabolic disturbances can precede weight gain, even if the latter still remains the hallmark of AAPs use. In fact, AAPs interfere profoundly with glucose and lipid homeostasis acting mostly on hypothalamus, liver, pancreatic β-cells, adipose tissue, and skeletal muscle. Their ac-tions on hypothalamic centers via dopamine, serotonin, acetylcholine, and histamine receptors affect neuropeptides and 5′ AMP-activated protein kinase (AMPK) activity, thus producing a supra-physiological sympathetic outflow augmenting levels of glucagon and hepatic glucose production. In addition, altered insulin secretion, dyslipidemia, fat deposition in the liver and adipose tissues, and insulin resistance become aggravating factors for MetS. In clinical practice, among AAPs, olan-zapine and clozapine are associated with the highest risk of MetS, whereas quetiapine, risperidone, asenapine and amisulpride cause moderate alterations. The new AAPs such as ziprasidone, lurasi-done and the partial agonist aripiprazole seem more tolerable on the metabolic profile. However, these aspects must be considered together with the differences among AAPs in terms of their efficacy, where clozapine still remains the most effective. Intriguingly, there seems to be a correlation between AAP’s higher clinical efficacy and increase risk of metabolic alterations. Finally, a multidisciplinary approach combining psychoeducation and therapeutic drug monitoring (TDM) is proposed as a first-line strategy to avoid the MetS. In addition, pharmacological treatments are discussed as well.
dc.format.extent26
dc.language.isoeng
dc.relation.ispartofPharmaceuticalsen
dc.rightsCopyright: © 2021 by the authors. 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 (https:// creativecommons.org/licenses/by/4.0/).en
dc.subjectAtypical antipsychotics (AAPs)en
dc.subjectClozapineen
dc.subjectDyslipidemiaen
dc.subjectG protein-coupled receptors (GPCRs)en
dc.subjectMetabolic syndrome (MetS)en
dc.subjectOlanzapineen
dc.subjectType 2 diabetesen
dc.subjectWeight gainen
dc.subjectRM Therapeutics. Pharmacologyen
dc.subjectMolecular Medicineen
dc.subjectPharmaceutical Scienceen
dc.subjectDrug Discoveryen
dc.subject.lccRMen
dc.titleAtypical antipsychotics and metabolic syndrome : from molecular mechanisms to clinical differencesen
dc.typeJournal itemen
dc.description.versionPublisher PDFen
dc.contributor.institutionUniversity of St Andrews. School of Physics and Astronomyen
dc.identifier.doihttps://doi.org/10.3390/ph14030238
dc.description.statusPeer revieweden


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