Intestinal mucosal environment and non-heme iron absorption

The intestinal mucosal environment and non-heme iron absorption refer to the physiological process and cellular machinery in the duodenum that facilitates the uptake of dietary iron. Non-heme iron, primarily in the ferric (Fe3+) form, must be reduced to ferrous (Fe2+) iron by the enzyme duodenal cytochrome b (Dcytb) before being transported across the apical membrane by divalent metal transporter 1 (DMT1) (McKie et al., 2001; Gunshin et al., 1997). Once inside the enterocyte, iron is either stored in ferritin or exported into the bloodstream via ferroportin, the only known mammalian iron exporter (Donovan et al., 2000). This export process is tightly regulated by the liver-derived hormone hepcidin, which binds to ferroportin and induces its degradation to limit iron entry during systemic overload or inflammation (Nemeth et al., 2004). This system is critical for maintaining systemic iron homeostasis, and its dysfunction is central to the pathogenesis of iron deficiency anemia and iron overload disorders like hereditary hemochromatosis. Pharmacological interventions typically aim to either supplement iron levels using oral or intravenous iron salts or modulate the regulatory pathways using novel agents like hepcidin mimetics (Camaschella et al., 2020).

Other names

Intestinal iron absorptionNon-heme iron uptake pathwayDuodenal iron transport

Modulation of iron transport proteins (e.g., DMT1, Ferroportin) and regulatory hormones (e.g., Hepcidin) to control systemic iron levels.