Abstract: Background: The prevalence of childhood obesity has increased during the last few years in many parts of the world. It has been suggested that obesity results from the interaction between genetic and environmental factors. Vitamin D receptor (VDR) gene polymorphism is associated with several conditions involving postnatal growth, insulin sensitivity and Body Mass Index (BMI). Objective: The aim of the present study was to assess the genetic contribution of VDR polymorphisms to the pathogenetic mechanism of obesity. Methodology: The study included 110 children (50 obese and 60 control), 6-16 years old, recruited from Al-Azhar University Hospital, Damietta; during the period from July, 2015 to April, 2016. For each child, three single nucleotide VDR gene polymorphisms were genotyped: FokI, ApaI and TaqI using the Restriction Fragment Length Polymorphism (RFLP) technique. Results: Obese children had significantly low vitamin D (28.7±7.9 ng mL–1) than control group (32.4±4.2 ng mL–1, p = 0.002). Regarding genotype distributions, no significant difference between cases and controls was observed in genotype and allele frequencies of VDR-FokI and VDR-ApaI. For the TaqI polymorphism, there were significant differences in genotype frequencies of VDR-TaqI between obesity and control groups (p = 0.039) (OR for ‘tt’ allele = 3.47, 95% CI: 1.1-10.7). The ‘t’ allele distribution in the obesity group was significantly higher than control group (p = 0.003) and the OR for ‘t’ was 2.33 (95% CI: 1.34-4.1). Among obesity-only children, homozygotes of the VDR-TaqI ‘tt’ variant were associated with increased triglyceride levels (p = 0.03) and HDL levels (p = 0.006). Conclusion: These results further support a role for VDR-TaqI polymorphism as risk factor for obesity and suggest its further validation inlarger independent populations as well as highlight a target for functional analysis towards therapeutic intervention in obese individuals.