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The Relationship of Leptin (+19) AG, Leptin (2548) GA, and Leptin Receptor Gln223Arg Gene Polymorphisms with Obesity and Metabolic Syndrome in Obese Children and Adolescents

  • Bilge, Serap (Department of Pediatrics, Gaziosmanpasa University Hospital) ;
  • Yilmaz, Resul (Department of Pediatrics, Gaziosmanpasa University Hospital) ;
  • Karaslan, Erhan (Department of Pediatrics, Gaziosmanpasa University Hospital) ;
  • Ozer, Samet (Department of Pediatrics, Gaziosmanpasa University Hospital) ;
  • Ates, Omer (Department of Biochemistry, Gaziosmanpasa University Hospital) ;
  • Ensari, Emel (Department of Medical Biology, Gaziosmanpasa University Hospital) ;
  • Demir, Osman (Department of Biostatistics, Gaziosmanpasa University Hospital)
  • Received : 2019.09.18
  • Accepted : 2021.01.22
  • Published : 2021.05.15

Abstract

Purpose: Obesity is defined as the abnormal or excessive accumulation of fat over acceptable limits. Leptin is a metabolic hormone present in the circulation in amounts proportional to fat mass. Leptin reduces food intake and increases energy expenditure, thus regulating body weight and homeostasis. Various polymorphisms are present in the leptin gene and its receptor. These polymorphisms may be associated with obesity. This study aimed to show the association of leptin (+19) AG, leptin (2548) GA, and Gln223Arg leptin receptor polymorphisms with obesity and metabolic syndrome in Turkish children aged 6-17 years, and to conduct further investigations regarding the genetic etiology of obesity. Methods: A total of 174 patients diagnosed with obesity and 150 healthy children who were treated at Tokat Gaziosmanpasa Medical School Hospital between September 2014 and March 2015 were included in this study. The ages of the children were between 6 and 17 years, and anthropometric and laboratory results were recorded. Genotyping of leptin (+19) AG, leptin (2548) GA, and leptin receptor Gln223Arg polymorphisms was performed by polymerase chain reaction. Results: An association between leptin receptor Gln223Arg gene polymorphism and obesity was detected. Conclusion: Further studies are needed to determine the role of genetic etiologies and to indicate the role of leptin signal transmission impairment in the pathogenesis of obesity. We hope that gene therapy can soon provide a solution for obesity.

Keywords

References

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