Mucosal block

Fig. 3. The mucosal block mechanism for the intestinal regulation and control of iron uptake into the blood...

Figure 6. Scheme of the consequences on iron.zinc interaction of a mucosal block regulation of iron transfer. If the site of iron.zinc competition is distal to the site of iron regulation (above) then iron sufficiency should reduce iron. zinc competition, increasing net zinc uptake. 

In monogastric species iron absorption takes place primarily in the upper small intestine (1). Not all the iron present in foods is absorbed into the body. In the normal adult with adequate stores of iron, usually less than 10% of the iron in foods is absorbed (2). Because of the body s limited capacity to excrete iron, the ability to refrain from absorbing unneeded iron is regulated in the duodenum and is referred to as the mucosal block (1). When the requirement for iron increases as in growth and pregnancy and in various disease and deficiency states, the mucosal block is modified and Increased iron absorption occurs. The explanation offered by Underwood (3) is as follows iron taken into the mucosal cell is converted to... 

At normal levels of iron intake, absorption requires uptake from the intestinal lumen by the mucosa and transfer from the mucosa to the portal blood. Both events are inversely affected by the state of body iron stores. In iron deficiency states, nonferrous metals such as cobalt and manganese, which have an ionic radius similar to that of iron and form octahedral complexes with six-coordinate covalent bonds, also are absorbed at an increased rate. Oral administration of a large dose of iron reduces (or temporarily inhibits) the absorption of a second dose of iron by the absorptive enterocytes even in the presence of systemic iron deficiency. The mechanism of mucosal block, which resists acquiring additional iron by the en-teroeytes with high amounts of intracellular iron, is not yet understood. It probably involves set points established in the enterocytes for iron recently consumed in the diet (dietary regulator). 

In all of these disorders, the gastrointestinal tract cannot limit absorption of iron to significant extent. Thus, the mucosal block responsible for keeping out unneeded iron on a daily basis is susceptible to disruption, perhaps at more than one point. Iron overload leads to... 

Ferritin also occurs in the cells of the intestinal mucosa where it has been thought to play some role in regulating the amount of dietary iron absorbed from the gut. From evidence of increased absorption of radioactive iron in humans with iron deficiency compared with normal subjects, who absorb very little, the idea of a mucosal block was... 

Fig. 3. The mucosal block theory of iron absorption. Iron taken up by the mucosal cell is converted to ferritin when the ferritin becomes physiologically saturated with iron, no more is taken up by the cell until iron is released from ferritin and transferred to the plasma...

Inasmuch as almost no iron is excreted, the mechanism controlling the levels of the iron reserves in the body must operate at the level of absorption [27, 28]. For many years the most popular theory invoked to explain the control of iron uptake was the theory of the mucosal block mechanism. The theory postulated the existence of a single, short-loop feedback mechanism within the cell of the intestinal mucosa. The absorbed iron would induce the de novo synthesis of apoferritin, and the apoferritin would then chelate iron to yield... 

Some explanation of the one-way absorption of iron was afforded by the mucosal block theory in which discharge of iron into the blood stream by the mucosal cells was assumed to be controlled by the concentration of iron in the serum. Serious objections to this concept were provided by the finding of high iron absorption in untreated pernicious anemia and in pyridoxine deficiency,in which conditions serum iron is high. Uptake... 

For demonstrating the absorption gradient and the so-called mucosal block, the method of Baker and Mollin (1955) is recommended. The hepatic uptake method too has proved valuable for studying the mucosal block and also for recording storage in the liver. It can be applied to subjects, normal and otherwise, without reference to their reliability in the matter of stool collection. 

The authors suggest that in addition to Castle s intrinsic factor there may be an intramural intestinal B12 acceptor (analogous to apoferritin in iron absorption) which may be responsible for the partial mucosal block to Bi2 absorption in the intestine of normal human beings. A similar mechanism may be responsible for limiting the amount of B12 which can be absorbed even with added intrinsic factor in patients with pernicious anemia (see page 163). 

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