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No association of LEPR Gln223Arg polymorphism with leptin, obesity or metabolic disturbances in children

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...

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Detalles Bibliográficos
Autores principales: Pyrzak, B, Wisniewska, A, Kucharska, A, Wasik, M, Demkow, U
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3521329/
https://www.ncbi.nlm.nih.gov/pubmed/20156757
http://dx.doi.org/10.1186/2047-783X-14-S4-201
Descripción
Sumario: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 ≥ 2 SDS) and the control group consisted of 41 children with BMI 20.0 ± 0.80 kg/m(2 )(BMI < 1.0 SDS). Polymorphism identification was performed in total genomic DNA using PCRRFLP 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.