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.


METHODS
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.


CONCLUSIONS
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.
Aeberli
I
I
Human Nutrition Laboratory, Institute of Food Science and Nutrition, ETH Zürich, Zürich, Switzerland. isabelle.aeberli@ilw.agrl.ethz.ch
Hurrell
R F
RF
Zimmermann
M B
MB
D000293:Adolescent; D023181:Antimicrobial Cationic Peptides / Q000097:blood*; D001682:Biological Availability; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D002648:Child; D004032:Diet; D004920:Erythropoiesis; D005260:Female; D064451:Hepcidins; D006801:Humans; D007501:Iron / Q000097:blood*; D000090463:Iron Deficiencies; D019266:Iron, Dietary / Q000008:administration & dosage / Q000097:blood* / Q000493:pharmacokinetics; D020738:Leptin / Q000097:blood*; D008297:Male; D009765:Obesity / Q000097:blood* / Q000150:complications / Q000453:epidemiology; D012016:Reference Values; D013557:Switzerland / Q000453:epidemiology; D014168:Transferrin / Q000378:metabolism*
D023181:Antimicrobial Cationic Peptides; D015415:Biomarkers; C578702:HAMP protein, human; D064451:Hepcidins; D019266:Iron, Dietary; D020738:Leptin; D014168:Transferrin; D002097:C-Reactive Protein; D007501:Iron