Hepcidin is the master regulator of systemic iron bioavailability in humans and plays a key
role in preventing iron overload. During pregnancy, iron is transported from the mother to the fetus across the placenta. However, the relationship between hepcidin and iron metabolism in the mother and the fetus remains unknown.
To elucidate this relationship, 40 women with singleton pregnanacies and their newborns were enrolled in this study. There were no mothers with active infection during the perinatal period.
Hemoglobin, serum iron, ferritin, and hepcidin levels were significantly higher in the fetuses than in the mothers, while transferrin and erythropoietin levels were significantly lower.
In the fetus, a significantly positive correlation between ferritin and hepcidin, and a significantly negative correlation between ferritin and transferrin showed sufficient accumulation of iron and prevention of an excessive iron transport. A positive correlation between erythropoietin and reticulocyte count indicates established erythropoiesis in the fetus at birth. Multiple regression analysis showed that fetal hepcidin levels were affected only by maternal serum iron (regression coefficient = -0.605, p=0.0060). Maternal and fetal iron metabolism were independently controlled, except for maternal iron transfer.
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