Iron deficiency anemia in inflammatory bowel disease

Figure 2 Role of hepcidin in the regulation of iron homeostasis. Fe³⁺ is reduced to Fe²⁺ by enterocyte brush border reductase Dcytb, transported across brush border membrane by DMT1. If iron demand is low, Fe²⁺ is stored as ferritin and sloughed with enterocytes. If iron demand is high, iron is oxidized by oxidase hephaestin and then exported into the plasma at the basolateral membrane by ferroportin[23]. Hepcidin binds to iron exporter, ferroportin 1, leading to its phosphorylation, internalization by binding to JAK 2 and lysosomal degradation, thus preventing iron release into the plasma[16]. DcytB: Duodenal ferric reductase; DMTI: Divalent metal transporter 1.