%0 Journal Article
%T Investigation of Associations between Obesity and LEP G2548A and LEPR 668A/G Polymorphisms in a Turkish Population
%A Server £¿ah£¿n
%A Ayd£¿n R¨¹stemo£¿lu
%A Ak£¿n Tekcan
%A T¨¹rker Ta£¿liyurt
%A Hasan G¨¹ven
%A Serb¨¹lent Y£¿£¿£¿t
%J Disease Markers
%D 2013
%R 10.1155/2013/216279
%X Objective. Obesity is a complex heterogeneous disease that is caused by genes, environmental factors, and the interaction between the two. The leptin (LEP) and leptin receptor (LEPR) genes have been evaluated for polymorphisms that could potentially be related to the pathophysiology of obesity and its complications. The aim of this study was to investigate the role of LEP G2548A and LEPR 668A/G polymorphisms in the pathogenesis of obesity. Subjects. The study included 127 patients with obesity and 105 healthy controls. Polymerase chain reaction and restriction fragment length analysis for LEP G2548A and LEPR 668A/G polymorphisms were applied. Results. There was no statistically significant difference in the genotype frequencies of the LEP gene polymorphism between patients and control groups ( ). We found a difference in the LEPR genotypes between patients and controls, but this was not statistically significant ( ). Additionally, we found an increased risk of obesity in the LEP/LEPR GG/GG combined genotype ( ). Conclusion. Our findings indicate that the LEP G2548A polymorphism is not a relevant obesity marker and that the LEPR 668A/G polymorphism may be related to obesity in a Turkish population. Further researches with larger patient population are necessary to ascertain the implications of LEP and LEPR polymorphisms in obesity. 1. Introduction Obesity is a complex heterogeneous disease that is caused by genes, environmental factors, and the interaction between the two [1]. Obesity is also a multifactorial condition, and many endocrine and inflammatory pathways are involved in its development and in obesity-related diseases [2]. Excess weight in obesity may come from muscles, bone, fat, and/or body water, but obesity specifically refers to having an abnormally high proportion of total body fat [3]. The World Health Organization defines ¡°overweight¡± as a body mass index (BMI) of 25 or more and ¡°obesity¡± as a BMI of 30 or more [4]. The prevalence of obesity has been stated as being near epidemic size [1¨C3, 5¨C7], and obesity has been associated with type II diabetes, hypertension, coronary artery disease, stroke, and many forms of cancer [8, 9]. Therefore, it is important that the underlying pathophysiology of obesity-related diseases is understood. Obesity results from the combined effects of genes, lifestyle, and the interactions of these factors [10], and both familial and nonfamilial factors play an important role in its development [1]. A genetic predisposition to obesity has been reported as a major risk factor for individuals [7]. With the
%U http://www.hindawi.com/journals/dm/2013/216279/