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Abstract Childhood obesity is a serious medical condition where excess body fat negatively affects a child’s health or well‑being. Healthcare professionals define obesity as increased adiposity on the basis of BMI, which is an excellent proxy for more direct measurement of body fat. BMI = weight (kg)/ height (m2). The normal range for BMI in children varies with age and sex. While a BMI above the 85th percentile is defined as overweight, a BMI greater than or equal to the 95th percentile is defined as obesity by Centers for Disease Control and Prevention (CDC). The prevalence of worldwide combined childhood overweight and obesity has increased from 4% in 1975 to 18% in 2016 for children between the ages of 5 and 19 years. The most recent prevalence of obesity and overweight in Egypt was reported in 2020; about 21.8% of the children were overweight and obese which is much close to the global prevalence. Obesity is a highly heritable multifactorial disease that places an enormous burden on human health. Many studies in humans indicate that obesity is related to interaction between genes and environmental factors. Interactive influences of environmental, genetic, and epigenetic factors are implicated in the pathogenesis of obesity. Leptin (LEP) is an endocrine hormone; it has several effects such as regulating food intake, energy expenditure, body weight and immune responses. LEP effects are mediated by its receptor (LEPR), which is located in the central nervous system and other tissues, including adipocytes and endothelial cells. Many studies showed that several of the polymorphisms of the LEPR genes are potentially related to the pathophysiology of obesity, metabolic syndrome and diabetes. |