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

Iron homeostasis during pregnancy.

Author information

1
Molecular, Cellular and Integrative Physiology Graduate Program and.
2
Center for Iron Disorders, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA.
3
Center for Iron Disorders, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA enemeth@mednet.ucla.edu.

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

PMID:
29070542
PMCID:
PMC5701706
DOI:
10.3945/ajcn.117.155812
[Indexed for MEDLINE]
Free PMC Article

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