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Background Vitamin D regulates cell proliferation and differentiation and exhibits immunoregulatory, antiangiogenic, and antioxidant characteristics. Vitamin D deficiency and vitamin D receptor (VDR) gene polymorphisms have been associated with an increased risk of metabolic syndrome components such as abdominal obesity, with both vitamin D deficiency and VDR gene polymorphisms contributing to its development. Obesity, metabolic disorders, and bone mass defects are associated with VDR alleles. The importance of VDR in the etiology of obesity has been related to the existence of the VDR polymorphisms  FokI, BsmI, ApaI , and  TaqI.  VDR expression in adipocytes affects energy metabolism and aids in obesity development. Objective The aim of this study was to examine a possible association between  BsmI  ( B, b  allele) polymorphism in the VDR gene and vitamin D status in obese Egyptian male medical students. Patients and methods This study was based on a comprehensive experiment known as “Nutritional Assessment of Medical Educational Students (NAMES)” that was completed in 2018 with 700 healthy participants (men and women). In total, out of the 700 participants 30 healthy men were enrolled in this study who matched our inclusion criteria. They attended Ain Shams University Hospital in Cairo between April 2019 and November 2020. This study was conducted at the Clinical Pathology Department of Ain Shams University Hospital, which is a part of the Faculty of Medicine. Participants were divided into two groups: Group I consisted of 12 obese men with nondeficient vitamin D levels (&gt; 20 ng/dl), and Group II consisted of 18 obese men with deficient vitamin D levels (20 ng/dl). Peripheral blood samples were collected into EDTA tubes from all groups, and DNA was extracted and purified using spin purification for PCR (QIA amp DNA Mini Kit). A commercial real-time polymerase chain reaction (PCR) kit with predesigned TaqMan probes was used to analyze the single nucleotide polymorphism (SNP) ( BsmI ) rs 1544410 in the VDR gene. Results No statistically significant relationship was observed between vitamin D levels and all InBody bioelectrical impedance characteristics, as well as  BsmI  gene polymorphism and all InBody bioelectrical impedance parameters (P &gt; 0.05). Regarding  Bb  and  BB  genotypes, no statistically significant difference was observed between Groups I and II. The prevalence of  BB  genotype was higher in vitamin-D-deficient individuals, and  Bb  genotype was more common among obese participants than  BB  genotype, which showed a higher prevalence of the “ b ” gene; however, these were not significant. Iron profile (iron level, ferritin level, TIBC, and transferrin saturation) and  BsmI  gene polymorphism showed no statistically significant relationship (P &gt; 0.05). Glycated hemoglobin (HbA1c) level and  BsmI  gene polymorphism showed a statistically significant relationship (P = 0.002), with a higher mean value among  Bb  genotype carriers than among  BB  genotype carriers. Eosinophil count showed a statistically significant difference between  BB  and  Bb  genotype carriers (P = 0.045), with a higher mean value among  Bb  genotype carriers than among  BB  genotype carriers.  Bsml  gene polymorphism showed no statistically significant relationship with any other complete blood count parameters (P &gt; 0.05.) Conclusion There was no significant relationship between VDR gene polymorphism ( BsmI ) and body mass index (BMI) nor between the different InBody bioelectrical impedance parameters. We noticed the prevalence of  BB  genotype among vitamin-D-deficient obese students and the frequency of the “ b ” allele among obese candidates according to the findings of our study. There was also no significant relationship between  BsmI  gene polymorphism and vitamin D levels. However,  BsmI  gene polymorphism and HbA1c levels and eosinophil count showed a relationship, which requires further investigation.

BsmI gene polymorphism of vitamin D receptor in obese Egyptian male medical students and its relationship with vitamin D deficiency