Editorial Review: The Control of Iron Balance by the Intestinal Mucosa

In this hypothetical model of intestinal function the ferritin apparatus of the absorptive epithelial cells provides the most important mechanism for day-to-day control of iron balance. Iron incorporated into epithelial ferritin cannot be released and therefore is lost when the cell is lost at the end of the life cycle. Information concerning the state of the body’s iron stores is conveyed to the intestine, perhaps by the concentration of plasma iron or iron-binding capacity. When the iron stores are replete the newly forming epithelial cells are constructed to contain a functional ferritin apparatus capable of synthesizing apoferritin and incorporating iron into ferritin, thus preventing its entering the body. However, this mechanism is not completely adequate to intercept all unneeded iron. When too much iron has bypassed the ferritin apparatus it may be intercepted by tissue macrophages in the villus and lost when these macrophages work their way into the lumen; or it may be loaded into newly forming villous epithelial cells thereby saturating a part of their ferritin capacity. Cells thus loaded would develop increased resistance to the incursion of dietary iron; they would also carry the ferritin iron away with them at the end of their life span. In iron deficiency the absorptive cells are constructed with a relative lack of ferritin apparatus so that dietary iron can pass freely into the cell and thence freely into the body.

In iron storage disease other populations of cells are used for excretion of iron. In general these are the glandular epithelial cells and tissue macrophages. Both varieties of cells are able to accept and store relatively large amounts of nonfunctional iron. They are deciduous cells which are shed from the internal surfaces of the body, and when they go their iron goes with them. The capacity of the excretory mechanism is not great, perhaps about 5 mg. per day. When the rate of introduction of iron into the body exceeds this capacity, siderosis of parenchymal tissues develops due to accumulation of excess iron.