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Fetal liver hepcidin supports acquisition of iron stores in utero

Lara Kammerer,G. Mohammad,Magda Wolna,P. Robbins,S. Lakhal-Littleton

Published 2019 in bioRxiv

ABSTRACT

The liver-derived hormone hepcidin (HAMP) controls systemic iron homeostasis by blocking the iron export protein ferroportin (FPN) in the gut and the spleen, the sites of iron absorption and recycling respectively. In the adult, disruption of HAMP expression or of FPN responsiveness to HAMP leads to increased liver iron stores. In the newborn, liver iron stores are important for supporting postnatal growth. However, it is not clear if fetal liver HAMP plays a role in regulating fetal iron stores. To address this question, we generated fetuses harbouring a ubiquitous or liver-specific knock-in the HAMP-resistant fpnC326Y allele, or liver-specific loss of the hamp gene. This was achieved using paternal inheritance in order to safeguard against the confounding effects of altered iron control in the mothers and in the maternal part of the placenta. We found that these fetuses had reduced liver iron stores compared with littermate controls. This was associated with marked increase in FPN in the fetal liver but not in the placenta. These results demonstrate that fetal liver HAMP operates in a cell-autonomous manner to increase fetal liver iron stores in utero. They also suggest that the function of FPN in the placenta is permissive of iron transport rather than regulatory.

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