Tags

Type your tag names separated by a space and hit enter

Iron homeostasis during pregnancy.
Am J Clin Nutr. 2017 Dec; 106(Suppl 6):1567S-1574S.AJ

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.

Authors+Show Affiliations

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

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

29070542

Citation

Fisher, Allison L., and Elizabeta Nemeth. "Iron Homeostasis During Pregnancy." The American Journal of Clinical Nutrition, vol. 106, no. Suppl 6, 2017, 1567S-1574S.
Fisher AL, Nemeth E. Iron homeostasis during pregnancy. Am J Clin Nutr. 2017;106(Suppl 6):1567S-1574S.
Fisher, A. L., & Nemeth, E. (2017). Iron homeostasis during pregnancy. The American Journal of Clinical Nutrition, 106(Suppl 6), 1567S-1574S. https://doi.org/10.3945/ajcn.117.155812
Fisher AL, Nemeth E. Iron Homeostasis During Pregnancy. Am J Clin Nutr. 2017;106(Suppl 6):1567S-1574S. PubMed PMID: 29070542.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Iron homeostasis during pregnancy. AU - Fisher,Allison L, AU - Nemeth,Elizabeta, Y1 - 2017/10/25/ PY - 2017/10/27/pubmed PY - 2017/12/19/medline PY - 2017/10/27/entrez KW - anemia KW - hepcidin KW - iron regulation KW - placenta KW - pregnancy SP - 1567S EP - 1574S JF - The American journal of clinical nutrition JO - Am J Clin Nutr VL - 106 IS - Suppl 6 N2 - 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. SN - 1938-3207 UR - https://www.unboundmedicine.com/medline/citation/29070542/full_citation DB - PRIME DP - Unbound Medicine ER -