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Vitamin D supplementation, the metabolic syndrome and oxidative stress in obese children

  • Tal Grunwald , Shruti Fadia , Bruce Bernstein , Matthew Naliborski , Shufang Wu and Francesco De Luca EMAIL logo
Published/Copyright: December 15, 2016

Abstract

Background:

Previous studies suggest that vitamin D may play a role in cardiovascular and metabolic health. Oxidative stress has also been implicated in the development of cardiovascular disease. Evidence suggests that vitamin D deficiency may contribute to the occurrence of oxidative stress. This study aimed to determine whether treatment and correction of vitamin D deficiency in obese children led to changes in their metabolic profile, independent of changes in adiposity. In addition, we aimed to determine whether vitamin D deficiency and oxidative stress are causally related in obese children.

Methods:

In the retrospective arm, chart review identified 32 obese children who experienced normalization of vitamin D deficiency or insufficiency with vitamin D supplementation. We then correlated laboratory and anthropometric data with vitamin D levels. In the prospective arm of the study, urinary 8-isoprostane and hydrogen peroxide were measured before and after correction of vitamin D deficiency/insufficiency and correlated to vitamin D levels in seven patients.

Results:

In our predominantly Hispanic population of obese children in an urban setting, we demonstrated a cause-effect relationship between vitamin D deficiency and oxidative stress. In contrast, we found no association between vitamin D status, adiposity, and markers of insulin sensitivity, nor any effect of vitamin D treatment on the same parameters.

Conclusions:

These discordant findings suggest a differential effect of vitamin D on cardiovascular risk factors such as oxidative stress and insulin resistance. To confirm these findings, further prospective studies with larger sample size and longer follow-up are warranted.


Corresponding author: Francesco De Luca, MD, Department of Pediatrics, Section of Endocrinology and Diabetes, St. Christopher’s Hospital for Children, 160 East Erie Avenue, Philadelphia, PA 19134, USA, Phone: 215-427-8101, Fax: 215-427-8105

  1. Author contributions: All the authors have accepted responsibility for the entire content of this submitted article and approved submission.

  2. Research funding: None declared.

  3. Employment or leadership: None declared.

  4. Honorarium: None declared.

  5. Competing interests: The funding organization(s) played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

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Received: 2016-5-26
Accepted: 2016-11-4
Published Online: 2016-12-15
Published in Print: 2017-4-1

©2017 Walter de Gruyter GmbH, Berlin/Boston

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  2. Editorial
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