Plasma hepcidin is a modest predictor of dietary iron bioavailability in humans, whereas oral iron loading, measured by stable‐isotope appearance curves, increases plasma hepcidin

Abstract

Plasma hepcidin appears to be a major regulator of iron absorption and homeostasis, but there are few data in humans.We aimed to see if circulating hepcidin predicted iron bioavailability and to measure the plasma hepcidin response to varying amounts of absorbed iron.In study 1, women (n = 98) with serum ferritin concentrations < 25 or > 40 μg/L were given stable isotope–labeled meals with ferrous sulfate (FeSO4), ferrous fumarate (FeC4H2O4), or ferric pyrophosphate (FePPi). Then, plasma hepcidin and iron absorption were measured. In study 2, iron‐sufficient men (n = 4) were given oral doses of 3.8 mg and 60 mg iron as labeled FeSO4. The stable isotope appearance and the plasma hepcidin curve were measured over 6 h.In study 1, plasma hepcidin and ferritin strongly correlated (r = 0.79, P < 0.001). Plasma hepcidin significantly, but modestly, predicted iron bioavailability from FeSO4 and FeC4H2O4 (r = 20.51 and 20.46, respectively; P < 0.0001) but not from FePPi (r = 20.30, P = 0.056). In study 2, the 3.8 mg dose increased circulating absorbed iron to 0.42 μmol/L but did not increase plasma hepcidin. The 60 mg dose increased mean circulating absorbed iron to 5.9 μmol/L and produced a ~30% increase in plasma hepcidin at 6 h (P < 0.01).Plasma hepcidin is only a modest predictor of dietary iron bioavailability. Oral iron loading increases circulating hepcidin.The ETHZ and DSM Nutritional Products financially supported this study.