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Abstract Body weight is regulated by numerous physiological mechanisms that maintain balance between energy intake and energy expenditure. Thus, any factor that raises energy intake or decreases energy expenditure by even a small amount will cause obesity in the long-term. Leptin is a 16 kDa protein synthesized mainly by adipose tissue and was originally identified as the gene defect responsible for the obesity syndrome. Circulating leptin levels are directly related to adipose tissue mass. High leptin levels signal the presence of sufficient energy stores to sites in the central nervous system, which respond by reducing appetite and increasing energy expenditure, preventing severe obesity. The aim of this study was to investigate the competence of phagocytic functions (intracellular killing) in obese children and its relation to their serum leptin. All enrolled children were subjected to a detailed interview and full history taking, detailed clinical examination, anthropometric measures, Laboratory assessment for CBC, serum leptin, DHR test. The results were tabulated, graphically represented and analyzed using appropriate computer statistical methods. Anthropometric measurements (weight, height, BMI, waist circumference, hip circumference, and waist/hip ratio) which are increased by obesity and they are correlated positively significant to BMI (the surrogate of obesity). There is statistically significant difference between obese patient and non-obese control group regarding anthropometric measurements (weight, height, BMI, waist circumference, hip circumference, and waist/hip ratio) which are higher in obese than non-obese group and they are correlated positively significant to BMI (the surrogate of obesity). Our study shows that frequency of infection is higher in obese patient group than lean control group and also correlated positively with serum leptin. There is no statistically significant correlation between serum leptin hormone and gender or age of subjects. |