Non-heme dietary absorption pathway

The Non-heme dietary absorption pathway refers to the molecular and cellular mechanisms by which non-heme iron, predominantly from plant-based foods, is absorbed in the small intestine. This process mainly occurs in the duodenum and involves several key steps: non-heme iron (mostly ferric, Fe³⁺) is first reduced to ferrous iron (Fe²⁺) on the enterocyte surface by a ferric reductase enzyme, duodenal cytochrome B (Dcytb). The reduced ferrous iron is then transported into enterocytes via the divalent metal transporter 1 (DMT1). Inside the cell, iron can be stored in ferritin or exported to the bloodstream via ferroportin. The efficiency of non-heme iron absorption is influenced by dietary enhancers (such as vitamin C, which reduces ferric to ferrous iron and forms soluble complexes) and inhibitors (such as phytates, polyphenols, calcium, and certain proteins)[1][3][4][5]. The pathway is regulated by systemic iron requirements and the peptide hormone hepcidin, which modulates iron transporter availability and activity. Note: If you are searching for a specific protein or molecular target within this pathway, such as "Divalent metal transporter 1 (DMT1)", "Duodenal cytochrome B (Dcytb)", or "Ferroportin (IREG1)", those would be canonical therapeutic or molecular targets. The name "Non-heme dietary absorption pathway" is overly broad and best classified as a physiological process, not a molecule or specific target[1][4].

Other names

Non-heme iron absorption pathwayNonheme iron uptakeNon-haem iron transportIntestinal non-heme iron absorption

Enhancement of absorption (by reducing agents like vitamin C); competitive inhibition (by other divalent metals, phytates, polyphenols)