Background. The association of ADV-36 infection and obesity has been reported in children. The objective of this study was to examine the hypothesis that the association between ADV-36 infection and adiposity may be mediated by sub-optimal vitamin D status of the host.Methods. Ninety one apparently healthy children in different weight categories (normal weight: 33, overweight: 33, obesity: 25) aged 5-18 years were randomly selected from the registered population at National Food and Nutrition Surveillance Program (NFNS). The groups were matched based on age and sex. Anthropometric, biochemical and serological assessments were performed.Results. The amount of anti-ADV36-Ab increased whereas circulating concentrations of 25(OH)D decreased across BMI categories with higher amounts in children with normal weight than in children with overweight and obesity (31.0±16.4, 22.5±10.5 and 21.9±9.8 nmol/L, respectively, p=0.004).Logistic regression analysis revealed that for each unit increment of anti-ADV36-Ab, the chance of increase in weight was 8.5 times (OR: 8.5, p=0.029). Interestingly, when 25(OH)D was introduced into the model, anti-ADV36-Ab was no longer the predictor of weight increment and the chance of increase in weight reduced 5% for each unit increase in 25(OH)D concentration (OR: 0.95, p=0.012).Conclusion. It is suggested that ADV36-induced lipogenesis may be mediated by vitamin D deficiency in children with obesity.
BackgroundContributors to childhood obesity are in the "obesogenic environment" of the children including all those aspects in the child's environment that encourages him or her to eat more (usually unhealthy) foods and to have less physical activity (1). One of the proposed potential contributors to obesity is suboptimal vitamin D status. Detection of vitamin D receptor (VDR) and its signaling pathways in adipose tissue indicated that vitamin D could potentially affect development, metabolism and functions of body fat mass (2). Laboratory in vitro studies demonstrated the effect of calcitriol (1,25(OH) 2 D 3 ), the active form of the vitamin, and its inactive metabolites on adipogenesis in murine 3T3-L1 cell line. While VDR knock out (VDR-/-) and 1-α-hydroxylase knock out (CYP27B1 -/-) mice were highly resistant to weight gain due to dietary intake, the over-expression of human VDR in adipose