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Published online by Cambridge University Press: 15 April 2020
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).
Metabolic profiles, LEP, LEPR gene polymorphisms and the gene expressions of LEP, LEPR and PPARg2 were studied in SCH patients and controls.
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).
Leptin receptor, leptin and PPARg2 genes could be potential risk factors in developing metabolic adversities in SCH.
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