Effects of olanzapine treatment on lipid profiles in patients with schizophrenia: a systematic review and meta-analysis

Li, Rong; Zhang, Yiqi; Zhu, Wenqiang; Ding, Chen; Dai, Wenjie; Su, Xianwei; Dai, Wen; Xiao, Jianru; Xing, Zhenhua; Huang, Xiansheng

doi:10.1038/s41598-020-73983-4

Cited by 21 publications

(25 citation statements)

References 67 publications

(80 reference statements)

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“…Thus, hypertriglyceridemia is regarded as the central olanzapine-induced dyslipidemia. Similarly, our human and animal data in this study indicated that hypertriglyceridemia was the most representative olanzapine-induced dyslipidemia, as evidenced by our previous meta-analysis study [7]. To date, however, the mechanisms underlying olanzapine-induced hypertriglyceridemia remain to be elucidated.…”

Section: Discussionsupporting

confidence: 80%

“…Olanzapine is one of the most prescribing atypical antipsychotics for schizophrenia patients [3] and produces overt dyslipidemia that remarkedly increases the morbidity and mortality of coronary heart disease (CHD) [4, 5]. Previous studies have shown that olanzapine-induced dyslipidemia is characterized with elevation of plasma triglycerides, low-density lipoprotein cholesterol (LDL-C) and total cholesterol, as well as reduction of high-density lipoprotein cholesterol (HDL-C) [6,7]. Of note, hypertriglyceridemia dramatically increases the CHD risk for schizophrenia patients [8-10].…”

Section: Introductionmentioning

confidence: 99%

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Olanzapine inhibits hepatic apolipoprotein A5 secretion inducing hypertriglyceridemia in schizophrenia patients and mice

Huang

Zhang

Zhu

et al. 2021

Preprint

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Olanzapine, an antipsychotic drug, was reported to induce hypertriglyceridemia, whereas the underlying mechanism remains incompletely understood. This study was to determine the role of apolipoprotein A5 (apoA5) in olanzapine-induced hypertriglyceridemia. In this study, 36 drug-naive and first-episode schizophrenic adult patients (aged 18–60 years) in a multi-center clinical trial (ClinicalTrials.gov NCT03451734) were enrolled. Before and after olanzapine treatment, plasma lipid and apoA5 levels were detected. Moreover, 21 female C57BL/6 J mice (8 weeks old) were divided into 3 groups (n = 7/each group): low-dose olanzapine (3 mg/kg/day), high-dose olanzapine (6 mg/kg/day) and control group. After 6 weeks, plasma glucose, lipids and apoA5 as well as hepatic apoA5 protein and mRNA expression in these animals were detected. In our study in vitro, primary mouse hepatocytes and HepG2 cells were treated with olanzapine of 25, 50, 100 μmol/L, respectively. After 24 hours, apoA5 protein and mRNA levels in hepatocytes were detected. Our study showed that olanzapine treatment significantly increased plasma triglyceride levels and decreased plasma apoA5 levels in these schizophrenic patients. A significant negative correlation was indicated between plasma triglyceride and apoA5 levels in these patients. Consistently, olanzapine dose-dependently increased plasma triglyceride levels and decreased plasma apoA5 levels in mice. Surprisingly, an elevation of hepatic apoA5 protein levels was detected in mice after olanzapine treatment, with no changes of APOA5 mRNA expression. Likewise, olanzapine increased apoA5 protein levels in hepatocytes in vitro, without changes of hepatocyte APOA5 mRNA. Therefore, our study provides the first evidence about the role of apoA5 in olanzapine-induced hypertriglyceridemia. Furthermore, plasma apoA5 reduction, resulting in hypertriglyceridemia, could be attributed to olanzapine-induced inhibition of hepatic apoA5 secretion.

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Section: Discussionsupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Olanzapine inhibits hepatic apolipoprotein A5 secretion inducing hypertriglyceridemia in schizophrenia patients and mice

Huang

Zhang

Zhu

et al. 2021

Preprint

Self Cite

View full text Add to dashboard Cite

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“…Evidence indicates that patients with schizophrenia are more likely to experience inadequate healthcare, receive fewer assessment for medical and physical conditions, and inadequate treatment as compared to the general population [ 8 , 21 ]. Providing good quality care and carrying out comprehensive, systematic assessment for patients with mental illnesses is a core clinical proficiency and a fundamental and integral part of comprehensive management.…”

Section: Discussionmentioning

confidence: 99%

“…Development of dyslipidemia in schizophrenia is associated with advanced age, cognitive impairment, lifestyle patterns, poor diet, poverty, the treatment of schizophrenia (antipsychotic medications), and imbalanced blood lipid components. The presence of dyslipidemia causes significant risk to heart disease, stroke and other cardiovascular-related morbidity, and mortality [ 8 ]. The relationships between schizophrenia and subsequent dyslipidemia (dyslipidemia after the diagnosis of schizophrenia) play a crucial role in clinical management of both schizophrenia and cardiovascular disease.…”

Section: Introductionmentioning

confidence: 99%

“…Occurrence of dyslipidemia in patients with schizophrenia is often neglected or disregarded by both mental health professionals and patients themselves. This accompanied by suboptimal physical health care in these patients may have accounted for the high prevalence of cardiovascular disease and mortality [ 8 , 24 ]. Early detection of dyslipidemia permits opportunity to identify the underlying medical cause and implements interventions against predisposing and precipitating risk factors.…”

Section: Introductionmentioning

confidence: 99%

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Subsequent Dyslipidemia and Factors Associated with Mortality in Schizophrenia: A Population-Based Study in Taiwan

Hsu

Ouyang

2021

Healthcare

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Background: Persons with schizophrenia are at greater risk of developing subsequent medical conditions. To date, few studies have examined comprehensively the risks, mortality and survival rates in schizophrenia and subsequent dyslipidemia over different time periods. The objective of this study was to evaluate the occurrence of subsequent dyslipidemia after the diagnosis of schizophrenia, and factors associated with mortality and survival rate in patients with schizophrenia. Methods: We used a population-based cohort from Taiwan National Health Insurance Research Database, to investigate in patients whom were first diagnosed with schizophrenia during the period from 1997 through 2009, the risk of subsequent dyslipidemia during follow-up. Cumulative incidences and hazard ratios after adjusting for competing mortality risks were calculated. Results: A total of 20,964 eligible patients were included. Risks (i.e., comorbidity) and protective factors (i.e., statin use) have significant impacts on mortality. The mortality exhibits a U-shaped pattern by age. After 50, the risk of death increases with age. Risk of mortality before 50 increases with a decrease in age. Risks differed by the duration time to subsequent dyslipidemia after schizophrenia. Mean duration was 63.55 months in the survive group, and 43.19 months in the deceased group. The 5-, 10-, and 15-year survival rates for patients with schizophrenia and subsequent dyslipidemia were 97.5, 90, and 79.18%, respectively. Conclusion: Early occurrence of subsequent dyslipidemia is associated with increased overall mortality in patients with schizophrenia.

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Olanzapine‐induced weight gain and lipid dysfunction in mice between different gender

Zhu,

Zhao,

Chao

et al. 2024

Biomedical Chromatography

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As one of the most common antipsychotics, olanzapine may cause metabolic‐related adverse effects, but it is still unknown how olanzapine alters lipid metabolism. In this study, we found that olanzapine‐treated mice showed varying degrees of dyslipidemia, which was particularly pronounced in female mice. Based on ultra‐performance liquid chromatography–quadrupole time‐of‐flight–MS (UPLC–Q‐TOF–MS) technology and lipid metabolomics, we mapped the changes in lipid metabolism in olanzapine‐treated mice and then compared the changes in lipid metabolism between male and female mice. There were 98 metabolic differentiators between the olanzapine‐treated and control groups in females and 79 in males. These metabolites were glycerolipids, glycerophospholipids, fatty amides, and sphingolipids, which are involved in glycerolipid metabolism, glycerophospholipid metabolism, and fatty acid metabolism. These results suggest that olanzapine‐induced changes in the levels of lipid metabolites are closely associated with disturbances in lipid metabolic pathways, which may underlie lipemia. This lipidome profiling study not only visualizes changes in lipid metabolism in liver tissue but also provides a foundation for understanding the regulatory pathways and mechanisms involved in olanzapine‐induced lipid metabolism disorders. Furthermore, this study demonstrates differences in lipid metabolism between males and females, providing a reference for clinical treatment regimen selection.

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Effects of olanzapine treatment on lipid profiles in patients with schizophrenia: a systematic review and meta-analysis

Cited by 21 publications

References 67 publications

Olanzapine inhibits hepatic apolipoprotein A5 secretion inducing hypertriglyceridemia in schizophrenia patients and mice

Olanzapine inhibits hepatic apolipoprotein A5 secretion inducing hypertriglyceridemia in schizophrenia patients and mice

Subsequent Dyslipidemia and Factors Associated with Mortality in Schizophrenia: A Population-Based Study in Taiwan

Olanzapine‐induced weight gain and lipid dysfunction in mice between different gender

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