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High circulating MIF levels indicate the association with atypical antipsychotic-induced adverse metabolic effects
Xi Chen1,2,3, Pingyi Gao2, Yadan Qi2
1Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Abstract:
Atypical antipsychotics (AAPs) are primary medications for schizophrenia (SZ). However, their use is frequently associated with the development of adverse metabolic effects, and the mechanisms behind these negative effects remain inadequately elucidated. To investigate the role of macrophage migration inhibitory factor (MIF) in regulating antipsychotic-induced metabolic abnormalities, between 2017 and 2020, a cross-sectional study was conducted, involving 142 healthy individuals and 388 SZ patients undergoing treatment with either typical antipsychotic (TAP) or AAP medications. Symptoms of SZ patients were evaluated using the Positive and Negative Syndrome Scale (PANSS), and measurements of metabolic indices and plasma MIF levels were performed on all individuals. A significant increase in plasma MIF levels was observed in groups receiving five major AAP monotherapies in comparison to healthy controls (all p < 0.0001). There was no such increase shown in the group receiving TAP treatment (p > 0.05). Elevated plasma MIF levels displayed a notable correlation with insulin resistance (β = 0.024, p = 0.020), as well as with the levels of triglycerides (β = 0.019, p = 0.001) and total cholesterol (β = 0.012, p = 0.038) in the groups receiving AAPs. However, while the TAP group also displayed certain metabolic dysfunction compared to healthy controls, no significant association was evident with plasma MIF levels (all p > 0.05). In conclusion, plasma MIF levels exhibit a distinctive correlation with metabolic abnormalities triggered by AAPs. Hence, there is potential for further development of MIF as a distinctive marker for monitoring adverse metabolic effects induced by AAPs in clinical settings.
Insights
Atypical antipsychotics increase macrophage migration inhibitory factor (MIF) levels, correlating with metabolic issues like insulin resistance and high cholesterol. MIF may serve as a marker for monitoring these adverse effects in schizophrenia patients.
Area of Science:
- Neuroscience
- Metabolic Disorders
- Pharmacology
Background:
- Atypical antipsychotics (AAPs) are crucial for schizophrenia (SZ) treatment but cause adverse metabolic effects.
- The mechanisms underlying these metabolic abnormalities induced by AAPs are not fully understood.
- Macrophage migration inhibitory factor (MIF) is implicated in inflammatory and metabolic processes.
Purpose of the Study:
- To investigate the association between macrophage migration inhibitory factor (MIF) and antipsychotic-induced metabolic abnormalities.
- To compare MIF levels and metabolic profiles in schizophrenia patients treated with AAPs versus typical antipsychotics (TAPs) and healthy controls.
Main Methods:
- A cross-sectional study involving 142 healthy individuals and 388 SZ patients (treated with TAPs or AAPs) from 2017-2020.
- Evaluation of schizophrenia symptoms using the Positive and Negative Syndrome Scale (PANSS).
- Measurement of plasma MIF levels and metabolic indices (including insulin resistance, triglycerides, and total cholesterol).
Main Results:
- Significantly elevated plasma MIF levels were observed in patients receiving five major AAP monotherapies compared to healthy controls (p < 0.0001).
- No significant increase in MIF levels was found in patients treated with TAPs (p > 0.05).
- Elevated MIF levels in AAP groups correlated significantly with insulin resistance (β=0.024, p=0.020), triglycerides (β=0.019, p=0.001), and total cholesterol (β=0.012, p=0.038).
Conclusions:
- Plasma MIF levels are distinctively correlated with metabolic abnormalities induced by atypical antipsychotics.
- MIF shows potential as a specific biomarker for monitoring adverse metabolic effects associated with AAP treatment.
- Further research could explore MIF-targeted interventions to mitigate antipsychotic-induced metabolic dysfunction.
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