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Overweight children have higher circulating hepcidin concentrations and lower iron status but have dietary iron intakes and bioavailability comparable with normal weight children

Abstract

Background:

Obesity increases the risk for iron deficiency, but the underlying mechanism is unclear. It is possible that overweight individuals may have lower dietary iron intake and/or bioavailability. Alternatively, obesity-related inflammation may increase hepcidin concentrations and reduce iron availability. Circulating hepcidin levels have not been compared in normal weight vs overweight individuals.

Objective:

The objective of this study was to compare iron status, dietary iron intake and bioavailability, as well as circulating levels of hepcidin, leptin and interleukin-6 (IL-6), in overweight vs normal weight children.

Design:

In 6–14-year-old normal and overweight children (n=121), we measured dietary iron intake, estimated iron bioavailability and determined body mass index s.d. scores (BMI-SDS). In all children (n=121), we measured fasting serum ferritin, soluble transferrin receptor (sTfR), C-reactive protein (CRP) and leptin; in a subsample, we measured IL-6 (n=68) and serum hepcidin (n=30).

Results:

There were no significant differences in dietary iron intake or bioavailability comparing normal and overweight children. The prevalence of iron-deficient erythropoiesis (an increased sTfR concentration) was significantly higher in the overweight than in the normal weight children (20 vs 6%, P=0.022, with sTfR concentrations of 4.40±0.77 and 3.94±0.88 mg l−1, respectively, P=0.010). Serum hepcidin levels were significantly higher in the overweight children (P=0.001). BMI-SDS significantly correlated with sTfR (P=0.009), serum hepcidin (P=0.005) and the three measures of subclinical inflammation, namely CRP (P<0.001), IL-6 (P<0.001) and leptin (P<0.001). In a multiple regression model, serum hepcidin was correlated with BMI-SDS (P=0.020) and body iron (P=0.029), but not with the inflammatory markers.

Conclusion:

Our findings indicate that there is reduced iron availability for erythropoiesis in overweight children and that this is unlikely due to low dietary iron supply but rather due to hepcidin-mediated reduced iron absorption and/or increased iron sequestration.

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Acknowledgements

We would like to thank all the children and families who participated in the study. We also thank Isabella Sciaroni, Nicole Beljean, Alexandra Uster and Evelyne Pflugi (ETH Zürich, Switzerland) who assisted with the study. Special thanks also go to Harold Tjalsma from http://www.hepcidinanalysis.com in Nijmegen for his assistance with the hepcidin measurements.

Each of the authors contributed to the study design and the statistical analysis of the data as well as the writing and editing of the paper. Data collection and laboratory analysis was done by IA.

This study was funded by the ETH Zurich.

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Correspondence to I Aeberli.

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Aeberli, I., Hurrell, R. & Zimmermann, M. Overweight children have higher circulating hepcidin concentrations and lower iron status but have dietary iron intakes and bioavailability comparable with normal weight children. Int J Obes 33, 1111–1117 (2009). https://doi.org/10.1038/ijo.2009.146

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