In plain words
Ferroportin is the protein that lets iron leave cells and enter the blood. It is found in the cells of the gut and in storage cells such as those in the liver and spleen. Its activity is controlled by a hormone called . When hepcidin is low, more ferroportin is active, and more iron is absorbed from food. During the second and third trimesters, hepcidin levels fall, so more iron can be taken up and sent to the baby and the mother's blood. This is part of how the body meets the rising iron demand of pregnancy. Ferroportin is not something you can see or feel. Its changes are one reason pregnancy iron needs are different from usual.
The deeper version
Ferroportin (SLC40A1) is the sole known cellular iron exporter, expressed on duodenal enterocytes, macrophages, and hepatocytes. Hepcidin binds ferroportin and triggers its internalization and degradation (Nemeth et al., Science, 2004). Hepcidin is suppressed in the second and third trimesters, raising fractional iron absorption and enabling mobilization of stores. Maternal iron absorption increases in pregnancy in tracer studies, though the magnitude varies. Inflammation raises hepcidin, which can impair iron release even when stores are adequate, a mechanism relevant to anemia of inflammation in pregnancy and the postpartum period.
Where it comes up
- Low iron and anemiaPregnancy: Your Body
- Iron-rich foods and how to absorb themPregnancy: Eating
- Anemia and exhaustion after birthPostpartum: Your Body
- Cravings and food aversionsPregnancy: Eating
What mothers here say about ferroportin
No one has posted under this term yet.
Sources
- Nemeth E et al. — Hepcidin regulates cellular iron efflux by binding to ferroportin and inducing its internalization. Science, 2004