Intestinal iron transport

Our current understanding of intestinal non-heme iron transport is illustrated in Figure 13.1. Iron absorption takes place in an acidic environment in the proximal small intestine, just distal to the gastric outlet. Most non-heme dietary iron is in the ferric (Fe3+) form. It is reduced to Fe2+ by a brush border ferrireductase, most likely the recently identified duo-

Ferroxidase Ferrireductase

Fig. 13.1 Current understanding of intestinal non-heme iron absorption

The cartoon shows an absorptive enterocyte from the duodenal epithelium, joined to adjacent cells by iron-impermeable tight junctions. The apical brush border is at the top and the basolateral surface is at the bottom. Dietary Fe3+ iron is probably reduced by the ferrireductase DCYTB to produce Fe2+ ion for transport. Fe2+ crosses the apical membrane through the action of DMT1 to enter the cell. There, iron is partitioned between storage and export; stored iron is ultimately lost from the body when the epithelial cells senesce and exfoliate into the gut lumen. Meanwhile, a fraction of the iron is exported across the basolateral membrane, probably by ferroportin. Hephaestin is a ferroxidase-like protein that aids in iron export, probably by reducing the Fe2+ iron leaving ferroportin to the Fe3+ form, which binds to plasma transferrin (TF).

Fig. 13.1 Current understanding of intestinal non-heme iron absorption

The cartoon shows an absorptive enterocyte from the duodenal epithelium, joined to adjacent cells by iron-impermeable tight junctions. The apical brush border is at the top and the basolateral surface is at the bottom. Dietary Fe3+ iron is probably reduced by the ferrireductase DCYTB to produce Fe2+ ion for transport. Fe2+ crosses the apical membrane through the action of DMT1 to enter the cell. There, iron is partitioned between storage and export; stored iron is ultimately lost from the body when the epithelial cells senesce and exfoliate into the gut lumen. Meanwhile, a fraction of the iron is exported across the basolateral membrane, probably by ferroportin. Hephaestin is a ferroxidase-like protein that aids in iron export, probably by reducing the Fe2+ iron leaving ferroportin to the Fe3+ form, which binds to plasma transferrin (TF).

denal cytochrome b (DCYTB). The Fe2+ ions pass through divalent metal transporter 1 (DMT1, formerly called Nramp2, DCT1), a membrane protein that allows iron to traverse the apical bilayer. DMT1 requires an acidic environment for its activity because it co-transports protons with iron atoms. Once it crosses the membrane, some of the iron is retained within the absorptive intestinal cells (enterocytes), and some is exported through the basolateral membrane through the action of a distinct transporter, ferroportin. A multicopper oxidase protein, hephaestin, facilitates basolateral transport, perhaps by oxidizing Fe2+ to Fe3+ to allow it to bind to the plasma iron carrier protein, transferrin.

The mechanisms controlling the rate of iron flux through this transport system are not well understood. However, it appears that only some of the dietary iron taken up by enterocytes passes into the plasma. Iron that is retained within the enterocytes is lost from the body when these cells finish their short lifespan and slough into the gut lumen. The partitioning of iron (that is, the process that governs how much enters the plasma and how much is retained within cells) is probably regulated, and likely plays an important role in determining the overall efficiency of iron absorption.

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