The hepcidin and 25-OH-Vitamin D levels in obese children as a potential mediator of the iron status

Aka S., Kılercık M., Arapoglu M., Semiz S.

Clinical Laboratory, vol.67, no.5, pp.1154-1162, 2021 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 67 Issue: 5
  • Publication Date: 2021
  • Doi Number: 10.7754/clin.lab.2020.200813
  • Journal Name: Clinical Laboratory
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, EMBASE, MEDLINE
  • Page Numbers: pp.1154-1162
  • Acibadem Mehmet Ali Aydinlar University Affiliated: Yes


© 2021 Verlag Klinisches Labor GmbH. All rights reserved.Background: Obesity is associated with the risk factors such as iron and vitamin D deficiencies. Increased risk of iron deficiency generally correlates with the high levels of serum hepcidin in obese children. Vitamin D deficiency was also linked to an increase in serum hepcidin levels. We aimed to compare iron parameters and investigate the hepcidin levels in obese and non-obese children. Methods: This study included 83 children and adolescents including obese (n = 35) and non-obese (n = 48). Laboratory values including serum iron levels, total iron-binding capacity, percentage of transferrin saturation, ferritin, reticulocyte parameters and high sensitivity C-reactive protein (hsCRP), hepcidin, 25-OH-Vitamin D were measured. Results: Average levels of hepcidin, hsCRP, and ferritin were found to be similar in both study groups. Serum iron levels, total iron-binding capacity, percentage of transferrin saturation, and 25-OH-vitamin D levels were significantly lower in the obese group. There was no statistically significant difference between hepcidin and 25-OH-vi-tamin D levels. Average hepcidin levels were detected to be similar in both groups (p = 0.580) whereas, 25-OH-vi-tamin D levels were significantly lower in the obese group (p < 0.001). A statistically negative correlation was observed between average BMI (body mass index) and serum iron level (r = -0.476; p < 0.001), BMI and transferring saturation (r = -0.467; p < 0.001), and BMI and 25-OH-vitamin D levels (r = -0.474; p < 0.001). Hence, no statistically significant relation was detected between hepcidin and 25-OH-vitamin D levels (r = 0.233; p = 0.084). Being female, vitamin D deficiency, and IRF (%) (Immature Reticulocyte Fraction) were found as independent risk factors for BMI increase due to logistic regression analyses. Conclusions: In conclusion, observed statistical associations and correlations do not prove a causal relationship between the hepcidin levels and iron deficiency but vitamin D deficiency seems likely to cause high BMI levels or in contrast, obesity may cause vitamin D deficiency in the children. No association was found between hepcidin, ferritin, and hsCRP levels with obesity in children. However, vitamin D deficiency was detected to cause a 5.3-fold increase in BMI levels. We suggest that there may be different mechanisms in obesity-related metabolic and hematological events. One can also envision that there is not enough time for the chronic inflammation processes to develop during childhood as opposed to those frequently seen in adult obese individuals.