ReviewFrontiers in psychiatry2023
Second-generation antipsychotics and metabolic syndrome: a role for mitochondria.
Review in Frontiers in psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Protein glycoxidation in neuropsychiatric disorders-from basic research to clinical practice.Redox biology · 2026Review
- A genetic atlas of relationships between circulating metabolites and liability to psychiatric conditions.Molecular psychiatry · 2026Article
- Prevalence and Healthcare Costs of Metabolic Disorders Among Individuals with Schizophrenia Following Initiation of Oral Antipsychotic Therapy.PharmacoEconomics - open · 2026Article
- Article
- Managing metabolic syndrome in bipolar disorder: multidisciplinary monitoring and treatment strategies.Frontiers in psychiatry · 2026Review
- Decoding psychotropic-induced metabolic disturbances: gut-brain axis, multi-omics, and nutrition-lifestyle integration.Frontiers in nutrition · 2026Review
- Beyond dopamine: KarXT and emerging mechanism-based therapies in schizophrenia.Frontiers in psychiatry · 2026Review
- Partners in plasticity: serotonergic glial interactions in brain circuit remodeling.Frontiers in neuroscience · 2026Review
- Linking the relationship between drug-induced osteoporosis and the gut microbiota.Frontiers in endocrinology · 2026Review
- The Role of GST Gene Polymorphic Variants in Antipsychotic-Induced Metabolic Disorders in Schizophrenia: A Pilot Study.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Antipsychotics and Change of Weight, Menstrual Cycle, and Metabolic Syndrome Components Among Schizophrenic Women: A 12-Week Longitudinal Prospective Study in Tien Giang, Vietnam.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Sleep and psychiatric disorders: Bidirectional interactions and shared neurobiological mechanisms.PLOS mental health · 2025Review
- Olanzapine and peripheral metabolic dysregulation: organ-resolved mechanisms, risk, and MASLD-aligned care pathways.Frontiers in pharmacology · 2025Review
- Current Evidence Regarding the Evaluation and Management of Neonatal Delirium.Current psychiatry reports · 2024Review
- Aripiprazole, but Not Olanzapine, Alters the Response to Oxidative Stress in Fao Cells by Reducing the Activation of Mitogen-Activated Protein Kinases (MAPKs) and Promoting Cell Survival.International journal of molecular sciences · 2024Article
- Metabolic Side Effects from Antipsychotic Treatment with Clozapine Linked to Aryl Hydrocarbon Receptor (AhR) Activation.Biomedicines · 2024Review
- Targeting Serotonin 5-HTAggression and violent behaviorArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.