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Iron absorption in the gastrointestinal (GI) tract is a tightly regulated physiological process that ensures adequate iron uptake to meet systemic needs while preventing toxicity. The primary site of iron absorption is the duodenum and upper jejunum, where both heme and non-heme dietary iron are taken up by enterocytes through distinct molecular mechanisms. This involves the reduction of ferric iron (Fe³⁺) to ferrous iron (Fe²⁺) by DCYTB, transport via DMT1, heme uptake via HCP1, intracellular storage as ferritin, and export via ferroportin regulated by hepcidin. Gastric acidity and dietary factors significantly modulate iron absorption. Dysregulation can lead to iron deficiency or overload syndromes.
Varies depending on the specific drug. Iron supplements directly increase iron availability. Antacids/PPIs reduce gastric acidity, decreasing iron absorption. Chelating agents bind iron, preventing its absorption or promoting its excretion.
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