Katherine R H Mortimer
Second-generation antipsychotics and metabolic syndrome: a role for mitochondria
Mortimer, Katherine R H; Katshu, Mohammed Zia Ul Haq; Chakrabarti, Lisa
Authors
Dr Mohammad Zia Ul Haq Katshu MOHAMMAD.KATSHU@NOTTINGHAM.AC.UK
CLINICAL ASSOCIATE PROFESSOR
Professor LISA CHAKRABARTI LISA.CHAKRABARTI@NOTTINGHAM.AC.UK
PROFESSOR OF MITOCHONDRIAL BIOLOGY
Abstract
Psychosis is a known risk factor for developing metabolic syndrome (MetS). The risk is even greater in patients who are taking second-generation antipsychotics (SGAs). SGAs exacerbate metabolic abnormalities and lead to a 3-fold increased risk of severe weight gain, type 2 diabetes, and cardiovascular disease in patients. Mitochondrial dysfunction is a hallmark of MetS. Mitochondria process glucose and fatty acids into ATP. If these processes are impaired, it can result in dyslipidaemia, hyperglycaemia and an imbalance between nutrient input and energy output. This leads to increased adiposity, insulin resistance and atherosclerosis. It is unclear how SGAs induce MetS and how mitochondria might be involved in this process. It has been found that SGAs impair cellular glucose uptake in liver, dysregulating glucose and fatty acid metabolism which leads to an accumulation of glucose and/or lipids and an increase reactive oxygen species (ROS) which target mitochondrial proteins. This affects complexes of the electron transport chain (ETC) to reduce mitochondrial respiration. While there is a suggestion that SGAs may interact with a variety of processes that disrupt mitochondrial function, some of the results are conflicting, and a clear picture of how SGAs interact with mitochondria in different cell types has not yet emerged. Here, we outline the current evidence showing how SGAs may trigger mitochondrial dysfunction and lead to the development of MetS.
Citation
Mortimer, K. R. H., Katshu, M. Z. U. H., & Chakrabarti, L. (2023). Second-generation antipsychotics and metabolic syndrome: a role for mitochondria. Frontiers in Psychiatry, 14, Article 1257460. https://doi.org/10.3389/fpsyt.2023.1257460
Journal Article Type | Article |
---|---|
Acceptance Date | Nov 10, 2023 |
Online Publication Date | Nov 24, 2023 |
Publication Date | Nov 24, 2023 |
Deposit Date | Nov 24, 2023 |
Publicly Available Date | Nov 24, 2023 |
Journal | Frontiers in Psychiatry |
Electronic ISSN | 1664-0640 |
Publisher | Frontiers Media |
Peer Reviewed | Peer Reviewed |
Volume | 14 |
Article Number | 1257460 |
DOI | https://doi.org/10.3389/fpsyt.2023.1257460 |
Keywords | Antipsychotics; psychosis; mitochondria; energy metabolism; metabolic syndrome |
Public URL | https://nottingham-repository.worktribe.com/output/27598221 |
Files
Fpsyt-14-1257460
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PDF
Publisher Licence URL
https://creativecommons.org/licenses/by/4.0/
Copyright Statement
© 2023 Mortimer, Katshu and Chakrabarti
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