Nikooyeh Bahareh, Hollis Bruce W, Neyestani Tirang R
Laboratory of Nutrition Research, National Nutrition and Food Technology Research Institute and Faculty of Nutrition Sciences and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Division of Neonatology, Department of Pediatrics, Medical University of South Carolina, Charleston, SC, 29425, USA.
BMC Pediatr. 2020 Jun 27;20(1):316. doi: 10.1186/s12887-020-02216-4.
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.
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.
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).
It is suggested that ADV36-induced lipogenesis may be mediated by vitamin D deficiency in children with obesity.
儿童中已报道腺病毒36型（ADV - 36）感染与肥胖之间存在关联。本研究的目的是检验以下假设：ADV - 36感染与肥胖之间的关联可能由宿主维生素D状态欠佳介导。
从国家食品和营养监测计划（NFNS）登记人群中随机选取91名5 - 18岁不同体重类别的健康儿童（正常体重：33名，超重：33名，肥胖：25名）。各小组按年龄和性别进行匹配。进行了人体测量、生化和血清学评估。
抗ADV36抗体量增加，而25(OH)D的循环浓度在不同BMI类别中降低，正常体重儿童的浓度高于超重和肥胖儿童（分别为31.0±16.4、22.5±10.5和21.9±9.8nmol/L，p = 0.004）。逻辑回归分析显示，抗ADV36抗体每增加一个单位，体重增加的几率为8.5倍（比值比：8.5，p = 0.029）。有趣的是，当将25(OH)D纳入模型时，抗ADV36抗体不再是体重增加的预测指标，且25(OH)D浓度每增加一个单位，体重增加的几率降低5%（比值比：0.95，p = 0.012）。
提示肥胖儿童中ADV36诱导的脂肪生成可能由维生素D缺乏介导。
