Nonheme iron absorption

Nonheme iron absorption refers to the process by which iron in the ferric (Fe³⁺) form, found in plant-based and fortified foods, is converted to absorbable ferrous (Fe²⁺) iron and transported into intestinal enterocytes, primarily in the duodenum. This process involves several proteins and is regulated by dietary components (e.g., enhancers: ascorbic acid; inhibitors: phytates, polyphenols) and systemic feedback via hepcidin. Nonheme iron must first be reduced by ferric reductases (e.g., duodenal cytochrome B) at the apical membrane, then transported by divalent metal transporter 1 (DMT1) into enterocytes, and finally exported into circulation by ferroportin under the regulatory influence of hepcidin[1][3]. Nonheme iron absorption is critical for iron balance but is not itself a single target or receptor. Key points: "Nonheme iron absorption" is a process, not a unique molecule or receptor[3]. The process involves several transporters and regulatory proteins (e.g., DMT1, duodenal cytochrome B, ferroportin, hepcidin)[2][3]. Common laboratory biomarkers for assessing its function/efficacy in vivo include serum ferritin, hemoglobin, and serum iron[1][5]. Drugs do not directly target "nonheme iron absorption" per se, but manipulation of dietary components, chelators, or systemic regulators (such as hepcidin modulators) can alter overall iron absorption[1][3]. Summary: "Nonheme iron absorption" cannot be classified as a canonical therapeutic target and therefore does not have a standardized molecular abbreviation or family; it is a physiological pathway involving multiple transporters and regulatory proteins rather than a single molecular entity[3].

Other names

Non-heme iron absorptionNonheme iron uptake