Abstract

BackgroundThe 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.MethodsNinety 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.ResultsThe 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).ConclusionIt is suggested that ADV36-induced lipogenesis may be mediated by vitamin D deficiency in children with obesity.

Highlights

  • The association of ADV-36 infection and obesity has been reported in children

  • A cohort study revealed that circulating concentrations of 25(OH) D, the main biomarker of vitamin D status, below 50 nmol/L was related to new onset obesity in adults [4]

  • Over 92 and 100% of the participants had undesirable vitamin D status according to Institute of Medicine (IOM) [37] and Endocrine Society Guideline [38], respectively (Table 1)

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Summary

Introduction

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. 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]. Despite some clinical trials showing the fat mass-decreasing and antiinflammatory effects of supplementary vitamin D in adults [5,6,7], the relationship between vitamin D deficiency and obesity is still like a “chicken and egg story” [8]

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