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Ferric ion absorption refers to the physiological process by which dietary ferric iron (Fe³⁺) is acquired, primarily in the duodenum[1][4][5]. Ferric iron is first reduced to the more soluble ferrous form (Fe²⁺) by a brush border membrane-bound ferric reductase (Dcytb) before transport into enterocytes through the divalent metal transporter 1 (DMT1)[1][2][4][5]. Once inside the enterocyte, iron can be stored in ferritin or exported across the basolateral membrane by ferroportin, an iron exporter, with the help of hephaestin (a ferroxidase that re-oxidizes Fe²⁺ to Fe³⁺)[1][2][4][5]. The process is tightly regulated by the hormone hepcidin, which controls ferroportin expression and hence iron absorption in response to systemic iron needs and inflammation[1][4][5]. Impaired regulation or mutations in any of these proteins can cause disorders such as iron deficiency anemia or hereditary hemochromatosis[1][2][4].
Reduction of Fe³⁺ to Fe²⁺ facilitates DMT1-mediated uptake; Chelation aids in solubility and transport.
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