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ORIGINAL RESEARCH COMMUNICATION |
1 From the Institute of Food Research, Norwich, United Kingdom (MAR and JRD); the University of East Anglia, Norwich, United Kingdom (RC and SJF-T); and the Department of Clinical Chemistry, Radboud University Nijmegen Medical Centre, Nijmegen, Netherlands (DWS). 2 Supported by a grant from the Food Standards Agency (London, UK) 3 Reprints not available. Address correspondence to SJ Fairweather-Tait, School of Medicine, Health Policy & Practice, University of East Anglia, Norwich NR4 7TJ, Norfolk, United Kingdom. E-mail: s.fairweather-tait{at}uea.ac.uk.
Background: Iron absorption is proposed to be regulated by circulating hepcidin, but, to date, little data are available to evaluate this relation in humans.
Objective: Stored samples from a human iron absorption study were used to test the hypothesis that differences in plasma hepcidin explain interindividual variation in iron absorption.
Design: Hepcidin-25 concentrations were measured in fasting samples from men aged
40 y (n = 33) recruited to a study investigating the relation between the HFE genotype, iron absorption, and iron status.
Results: Log iron absorption was negatively correlated with serum ferritin (r = –0.59, P < 0.001) and with plasma hepcidin (r = –0.55, P < 0.001) but was unaffected by genotype. There was a positive correlation (r = 0.82, P < 0.001) between hepcidin (mean: 2.3; range: 0.1–7.8 nmol/L) and ferritin (mean: 70; range: 9–208 µg/L). Multiple linear regression models showed that plasma hepcidin in isolation significantly predicted 36% of the interindividual variation in iron absorption.
Conclusions: Plasma hepcidin and serum ferritin concentrations are highly correlated, and, in the normal range of plasma hepcidin values, 36% of interindividual differences in iron absorption are explained by differences in circulating plasma hepcidin.
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