Maternal minihepcidin administration influences embryonic iron status. Mice treated with minihepcidins model inflammation-mediated upregulation of maternal hepcidin. (A) The relationship between maternal and fetal circulation, with maternal iron (Fe) delivered to the syncytiotrophoblast by transferrin (Tf) via transferrin receptor 1 (TfR1). Iron needed for placental function is retained, and remaining Fe is exported for transfer to the fetal circulation by the iron efflux protein, ferroportin (Fpn). (B) Administration of the highest-dose regimen decreases maternal serum iron. The placenta compensates by increasing TfR1 and decreasing Fpn to ensure placental Fe is adequate, to the detriment of the fetus. (C) Administration of the low-dose regimen produces modest decreases in fetal iron endowment despite the absence of changes in maternal or placental iron status.