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Open AccessReview

Hepcidin and Iron Homeostasis during Pregnancy

Department of Women, Children and Family Health Science, College of Nursing, University of Illinois at Chicago 845 S. Damen Ave., Room 814 (MC802), Chicago, IL 60612, USA
Division of Health Promotion Research, Department of Medicine, University of Illinois at Chicago, Chicago, IL 60608, USA
University of Illinois Cancer Center, 1747W. Roosevelt Rd. #416, Chicago, IL, 60608, USA
Sumter Family Health Center, 1278 N Lafayette Drive Sumter, SC 29150, USA
School of Nursing, Yale University, 100 Church Street South, New Haven, CT 06519, USA
UCLA, Department of Medicine, Center for Iron Disorders, University of California Los Angeles, CHS 52-239, 10833 Le Conte Ave. Los Angeles, CA 90095-1690, USA
Author to whom correspondence should be addressed.
Nutrients 2014, 6(8), 3062-3083;
Received: 15 May 2014 / Revised: 2 July 2014 / Accepted: 8 July 2014 / Published: 4 August 2014
(This article belongs to the Special Issue Iron Deficiency: Development, Implications and Treatment)
PDF [712 KB, uploaded 4 August 2014]


Hepcidin is the master regulator of systemic iron bioavailability in humans. This review examines primary research articles that assessed hepcidin during pregnancy and postpartum and report its relationship to maternal and infant iron status and birth outcomes; areas for future research are also discussed. A systematic search of the databases Medline and Cumulative Index to Nursing and Allied Health returned 16 primary research articles including 10 human and six animal studies. Collectively, the results indicate that hepcidin is lower during pregnancy than in a non-pregnant state, presumably to ensure greater iron bioavailability to the mother and fetus. Pregnant women with undetectable serum hepcidin transferred a greater quantity of maternally ingested iron to their fetus compared to women with detectable hepcidin, indicating that maternal hepcidin in part determines the iron bioavailability to the fetus. However, inflammatory states, including preeclampsia, malaria infection, and obesity were associated with higher hepcidin during pregnancy compared to healthy controls, suggesting that maternal and fetal iron bioavailability could be compromised in such conditions. Future studies should examine the relative contribution of maternal versus fetal hepcidin to the control of placental iron transfer as well as optimizing maternal and fetal iron bioavailability in pregnancies complicated by inflammation. View Full-Text
Keywords: hepcidin; pregnancy; iron regulation; inflammation hepcidin; pregnancy; iron regulation; inflammation

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This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Koenig, M.D.; Tussing-Humphreys, L.; Day, J.; Cadwell, B.; Nemeth, E. Hepcidin and Iron Homeostasis during Pregnancy. Nutrients 2014, 6, 3062-3083.

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