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

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. International Journal of Obesity ( 2009) 33, 1111-1117; doi:10.1038/ijo.2009.146; published online 28 July 2009