Effects of maternal iron status on placental and fetal iron homeostasis

Fetal and amniotic fluid iron homeostasis in healthy and complicated murine, macaque, and human pregnancy

“…Indeed, a transgenic mouse model of hepcidin overexpression confirmed that fetal hepcidin is capable of regulating placental ferroportin, causing severe fetal iron deficiency and decreased viability (26,27). Under normal physiological conditions, endogenous fetal hepcidin expression is low (26,27) and does not affect iron transfer across the placenta (22). However, certain clinical conditions, such as intraamniotic infection or inflammation (IAI), can induce fetal hepcidin (28).…”

“…During pregnancy, iron is critical for the development of the fetus and placenta and for maternal erythropoietic expansion (17,18). To accommodate these changes, maternal hepcidin is suppressed to nearly undetectable levels in the second and third trimesters (19)(20)(21)(22); this is thought to facilitate increased dietary iron absorption, release of iron from stores, and iron transfer to the fetus (23). Thus, inappropriately elevated maternal hepcidin, as would be expected during inflammation, could be detrimental by compromising iron availability for placental uptake and transfer to the fetus.…”

Iron deficiency anaemia in pregnancy: A contemporary review

“…16 Ferroportin delivers stored, dietary or recycled iron to blood plasma and is expressed at all sites involved in iron-plasma exchange, including the basolateral membrane of duodenal enterocytes, macrophages, hepatocytes and the basal surface of placental syncytiotrophoblasts facing the fetal circulation. 16,23 At each of these sites hepcidin causes intracellular degradation of ferroportin, thereby preventing iron export to blood plasma ( Figure 1). Changes in hepcidin levels can lead to rapid fluctuations in plasma iron concentrations.…”

“…A recent study evaluating mechanisms in murine and in vitro trophoblastic models of severe ID observed an unexpected response that prioritised placental iron retention over fetal iron transfer. 23 This response may have an evolutionary benefit to protect iron-dependent placental processes, and may provide overall benefit for the fetus despite diminishing fetal iron availability. This work also suggests that the fetus may be unable to compensate for maternal ID by increasing placental iron transfer.…”

“…This work also suggests that the fetus may be unable to compensate for maternal ID by increasing placental iron transfer. 23 Further studies are required to clarify the significance of these findings.…”