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This Article Full Text Full Text (PDF) All Versions of this Article: 296/4/R1063    most recent 90793.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Gambling, L. Articles by McArdle, H. J. Search for Related Content PubMed PubMed Citation Articles by Gambling, L. Articles by McArdle, H. J.

DEVELOPMENTAL PHYSIOLOGY AND PREGNANCY

Fetal iron status regulates maternal iron metabolism during pregnancy in the rat

¹Rowett Institute of Nutrition and Health and ²Biomathematics and Statistics Scotland, University of Aberdeen, Bucksburn Aberdeen, United Kingdom; ³Department of Biochemistry and Molecular Biology, Royal Free Hospital, London, United Kingdom; and ⁴Department of Hygiene and Human Nutrition, Agricultural University, Poznan, Poland

Submitted 24 September 2008 ; accepted in final form 21 January 2009

Iron metabolism during pregnancy is biased toward maintaining the fetal supply, even at the cost of anemia in the mother. The mechanisms regulating this are not well understood. Here, we examine iron deficiency and supplementation on the hierarchy of iron supply and the gene expression of proteins that regulate iron metabolism in the rat. Dams were fed iron-deficient diets for 4 wk, mated, and either continued on the deficient diet or an iron-supplemented diet during either the first half or the second half of their pregnancy. A control group was maintained on normal iron throughout. They were killed at 0.5, 12.5, or 21.5 days of gestation, and tissues and blood samples were collected. Deficiency and supplementation had differential effects on maternal and fetal hematocrit and liver iron levels. From early in pregnancy, a hierarchy of iron supply is established benefiting the fetus to the detriment of the mother. Transferrin receptor, transferrin receptor 2, and hepcidin mRNA expression were regulated by both iron deficiency and supplementation. Expression patterns showed both organ and supplementation protocol dependence. Further analysis indicated that iron levels in the fetal, and not maternal, liver regulate the expression of liver transferrin receptor and hepcidin expression in the mother.

placenta; deficiency; supplementation