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1043 – Expression Of Obesity Related Genes And Leptin Serum Levels Are Decreased In Turkish Schizophrenia Patients, Case-control Study

Published online by Cambridge University Press:  15 April 2020

G. Akan
Affiliation:
Medical Biology and Genetics, Istanbul Bilim University
O. Ozgen
Affiliation:
Medical Genetics, Istanbul University, Faculty of Medicine
A. Colak
Affiliation:
Biomedical Engineering, Bogazici University
S. Acar
Affiliation:
Bioengineering, Yildiz Technical University
F. Oncu
Affiliation:
Psychiatry Clinics, Turkish Ministry of Health Bakirkoy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery
D. Yesilbursa
Affiliation:
Psychiatry Clinics, Turkish Ministry of Health Bakirkoy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery
S. Turkcan
Affiliation:
Psychiatry Clinics, Turkish Ministry of Health Bakirkoy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery
F. Atalar
Affiliation:
Department Growth- Development and Pediatric Endocrinology, Child Health Institute, Istanbul University, Istanbul, Turkey

Abstract

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Antipsychotic medications can induce metabolic abnormalities (weight gain) in schizophrenia (SCH). Leptin receptor (LEPR), leptin (LEP) and peroxysome proliferator-activated receptor g2 (PPARg2) are the potential genetic determinants which might be liable of the metabolic dysregulation. The aim of this study was to evaluate the effect of LEP c.-2548G>A, LEPR p.Q223R polymorphisms and the impact of mRNA levels of LEP, LEPR, and PPARg2 along with the serum leptin levels on metabolic adversities in SCH patients (n=132) and controls (n=114).

Methods

Metabolic profiles, LEP, LEPR gene polymorphisms and the gene expressions of LEP, LEPR and PPARg2 were studied in SCH patients and controls.

Results

BMI, cholesterol and fasting glucose levels were higher in SCH patients compared to controls. LEP c.-2548 (GA+AA) genotypes were two fold lower in SCH patients versus controls (p< 0.05), and no significant difference was observed in LEPR p.Q223R genotypes. Interestingly, leptin serum levels were lower in SCH patients compared to controls (p< 0.05). Leptin, leptin receptor and PPARg2 gene expressions were found to be decreased in SCH patients compared to controls (p< 0.001, p< 0.001 and p≤0.05, respectively).

Conclusion

Leptin receptor, leptin and PPARg2 genes could be potential risk factors in developing metabolic adversities in SCH.

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Abstract
Copyright
Copyright © European Psychiatric Association 2013
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