Hepcidin secreted by the fetal liver does not appreciably affect placental iron delivery to the fetus through ferroportin (Fpn) on syncytiotrophoblast (STB) but does inhibit the efflux of iron from fetal hepatocytes through Fpn into fetal blood, presumably by an autocrine/paracrine mechanism. Retention of iron in fetal hepatocytes is required for effective fetal erythropoiesis in the liver, possibly because hepatocytes can transfer iron to adjacent erythroblasts. Professional illustration by Somersault18:24.

Hepcidin secreted by the fetal liver does not appreciably affect placental iron delivery to the fetus through ferroportin (Fpn) on syncytiotrophoblast (STB) but does inhibit the efflux of iron from fetal hepatocytes through Fpn into fetal blood, presumably by an autocrine/paracrine mechanism. Retention of iron in fetal hepatocytes is required for effective fetal erythropoiesis in the liver, possibly because hepatocytes can transfer iron to adjacent erythroblasts. Professional illustration by Somersault18:24.

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