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Review
. 2017 Dec;106(Suppl 6):1567S-1574S.
doi: 10.3945/ajcn.117.155812. Epub 2017 Oct 25.

Iron homeostasis during pregnancy

Allison L Fisher  1   2 , Elizabeta Nemeth  3
Affiliations
Review

Iron homeostasis during pregnancy

Allison L Fisher et al. Am J Clin Nutr. 2017 Dec.

Abstract

During pregnancy, iron needs to increase substantially to support fetoplacental development and maternal adaptation to pregnancy. To meet these iron requirements, both dietary iron absorption and the mobilization of iron from stores increase, a mechanism that is in large part dependent on the iron-regulatory hormone hepcidin. In healthy human pregnancies, maternal hepcidin concentrations are suppressed in the second and third trimesters, thereby facilitating an increased supply of iron into the circulation. The mechanism of maternal hepcidin suppression in pregnancy is unknown, but hepcidin regulation by the known stimuli (i.e., iron, erythropoietic activity, and inflammation) appears to be preserved during pregnancy. Inappropriately increased maternal hepcidin during pregnancy can compromise the iron availability for placental transfer and impair the efficacy of iron supplementation. The role of fetal hepcidin in the regulation of placental iron transfer still remains to be characterized. This review summarizes the current understanding and addresses the gaps in knowledge about gestational changes in hematologic and iron variables and regulatory aspects of maternal, fetal, and placental iron homeostasis.

Keywords: anemia; hepcidin; iron regulation; placenta; pregnancy.

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Figures

FIGURE 1
FIGURE 1
Hepcidin-ferroportin interaction controls systemic iron homeostasis. By causing degradation of Fpn, hepcidin decreases iron supply into plasma. Thus, lowering of maternal hepcidin during pregnancy increases iron bioavailability for placental transfer. Fetal hepcidin may control placental Fpn and the transfer of iron into fetal circulation. Fpn, ferroportin; RBC, red blood cell; Tf, transferrin.
FIGURE 2
FIGURE 2
Median (IQR) serum hepcidin concentrations in 31 women during pregnancy and postpartum. ***Compared with first-trimester values, P < 0.0001. Reproduced from reference with permission.
FIGURE 3
FIGURE 3
Mean (95% CI) Hb (A), Hct (B), and MCV (C) values during normal, unsupplemented pregnancy in 69 women. Reproduced from reference with permission. Hb, hemoglobin; Hct, hematocrit; MCV, mean corpuscular volume.
FIGURE 4
FIGURE 4
Geometric mean ± SEM serum ferritin concentrations during pregnancy in 63 women with iron supplementation and 57 women without iron supplementation. Reproduced from reference with permission. SF, serum ferritin.
FIGURE 5
FIGURE 5
Placental iron transport. On the apical side of the syncytiotrophoblast, maternal iron Tf binds to TfR1. After internalization, iron dissociates from Tf, is reduced by a ferrireductase, and is exported from the endosome into the cytoplasm, possibly via DMT1 or another transporter. Iron is exported from the syncytiotrophoblast by the iron exporter Fpn and eventually oxidized by a ferroxidase to be loaded onto fetal Tf or possibly transferred into fetal circulation as NTBI. How the iron is transported across the fetal endothelium is unclear. Cp, ceruloplasmin; DMT1, divalent metal transporter 1; Fpn, ferroportin; Heph, hephaestin; NTBI, non–transferrin-bound iron; STEAP, 6-transmembrane epithelial antigen of prostate; Tf, transferrin; TfR1, transferrin receptor 1; Zip, Zrt/Irt-like protein; Zp, zyklopen.
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