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No association of LEPR Gln223Arg polymorphism with leptin, obesity or metabolic disturbances in children
B Pyrzak1, A Wisniewska, A Kucharska
1Department of Pediatrics and Endocrinology, Warsaw Medical University, Warsaw, Poland. b.pyrzak@wum.edu.pl
Objective:
The aim of the study was to investigate whether the Gln223Arg in the leptin receptor may influence body weight, leptin concentration, and metabolic parameters in children.
Materials And Methods:
The examined group included 101 obese children (58 girls and 43 boys) with BMI 31.41 +/-5.03 kg/m(2) (BMI > or = 2 SDS) and the control group consisted of 41 children with BMI 20.0 +/-0.80 kg/m2 (BMI <1.0 SDS). Polymorphism identification was performed in total genomic DNA using PCR-RFLP method.
Results:
The distribution of genotypes LEPR was the following: in the obese group: AA - 20.8%, AG- 55.4%, GG-23.8 %; in the control group AA-31.7%, AG- 53.65%, GG-14.65%. Comparative analyses between AA homozygous children and carriers of G alleles did not confirm any relation between the analyzed polymorphism and BMI, leptin concentrations, and metabolic disturbances in children with obesity.
Conclusion:
In children with obesity we did not observe association of the LEPR Gln223Arg gene polymorphism with obesity, leptin, insulin resistance, and metabolic abnormalities.
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