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Regular “mucosal block” is characterized by decreased uptake of a normal iron load 3–72 h after the administration of excess iron (generally 10 mg) to iron-deficient animals. We found that short-acting mucosal block could be induced by much lower iron concentration and much shorter induction time than previously reported, without affecting levels of gene expression. A rapid endocytic mechanism was reported to decrease intestinal iron absorption after a high iron load, but the activating iron load and the time to decreased absorption were undetermined. We assessed the effects of 30–2,000 μg iron load on iron uptake in the duodenal loop of iron-deficient and iron-sufficient rats under anesthesia. One hour later, mucosal cellular iron uptake in iron-deficient rats administered 30 μg iron was 76.1%, decreasing 25% to 50.7% in rats administered 2,000 μg iron. In contrast, iron uptake by iron-sufficient rats was 63% (range 60.3–65.5%) regardless of iron load. Duodenal mucosal iron concentration was significantly lower in iron-deficient than in iron-sufficient rats. Iron levels in portal blood were consistently higher in iron-deficient rats regardless of iron load, in contrast to the decreased iron uptake on the luminal side. Iron loading blocked mucosal uptake of marginally excess iron (1,000 μg), with a greater effect at 15 min than at 30 min. The rapid induction of short-acting mucosal block only in iron-deficient rats suggests DMT1 internalization.

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Iron is a nutrient and its deficiency is the most frequent nutritional disorder worldwide, occurring in 4 to 5 billion people corresponding to about 70-80% of the world's population as estimated by the World Health Organization. However, an excess of iron increases oxidative stress and increases the risk of death and cancer; thus blood transfusion and supplementation should be used with caution. As there is no mechanism for deliberate iron excretion, the regulation of iron absorption in the small intestine is required to maintain total body iron balance and prevent excessive or deficient iron levels. Proteins involved in intestinal iron absorption were first identified in 1997. Molecular mechanisms of iron transport from the lumen of the small intestine to the portal blood through epithelial cells have been elucidated. In addition to long responses to iron deficiency in vivo, a short response exists for iron concentrations in the small intestine. This review describes regulatory mechanisms at the forefront of iron absorption, focusing on short acting mucosal block.