Arina fortificada

July 2002: (II)S3–S6

Food Iron Absorption and Its Importance for the Design of Food Fortification Strategies
Sean Lynch, M.D.
Dietary composition has a greater effect on iron bioavailability than it does on the amount of iron consumed because iron is widely distributed in the diet. The variation in individual iron intake is relatively small. For example, the mean daily intake reported in theThird National Health and Nutrition Examination Survey1 for adult women age 30 to 39 years is 12.73 mg. The standard error of the mean was only 0.36 mg. Even the lowest levels of iron intake would have provided an amount adequate for the needs of all menstruating women if it were all available for absorption. The body’s ability to extract the iron from many food items is limited, however, evenwhen the mechanisms controlling absorption are maximally up-regulated. The small proportion of heme iron (approximately 10 –15% of total dietary intake in western diets containing significant quantities of meat) derived from hemoglobin and myoglobin is always well absorbed. The efficiency with which the remaining 85% to 90% is assimilated may vary as much as 20-fold when measured in single-mealstudies.2 Because modifiers of absorption interact with each other, the variation in absorption in the context of a complete diet is less than that observed in single-meal studies suggests.3 Nevertheless, the bioavailability of iron from different diets may vary at least threefold. A clear understanding of factors that influence iron absorption is therefore critical to the design of effective fortificationstrategies. The mere addition of iron salts or elemental iron powders to foods rich in factors that render it unavailable to the mucosal uptake mechanisms is unlikely to be efficacious. Physiology of Iron Absorption Iron enters the body by way of specialized transport mechanisms in epithelial cells on the tips of the villi in the duodenum. At least two pathways are involved.4 Heme is taken upintact. The iron is then released from the porphyrin ring by heme oxygenase. All other forms of iron are transported into the cell by the divalent metal transporter (DMT1, previously named Nramp2 and DCT1), which is a proton symporter that transports ferrous iron and other divalent metals.5,6 The iron released from heme and the iron imported by DMT1 then appear to enter a common pathway that leadseither to the formation of ferritin and storage of the iron in the mucosal cell or export into the body at its basolateral surface. Most of the iron stored in ferritin is lost when the mucosal cell exfoliates. The mechanisms responsible for transport through the mucosal cell have not been identified, but a putative basolateral iron transporter, ferroportin 1 (also called Ireg 1 or MTP 1), has recentlybeen discovered.5 Coexpression of hephaestin, a cytosolic or transmembrane copper protein and ceruloplasmin, is required for the efficient transfer of iron out of the enterocyte and for binding to transferrin. Regulation of iron absorption is thought to occur primarily during entry of iron into the cell and at the time of exit into the body where it becomes bound to transferrin for delivery to thevarious organ systems. In the case of nonheme iron, uptake into mucosal cells is the primary site of regulation.7 When iron requirements are high, increased quantities of DMT1 are found on duodenal enterocyte surfaces. Dietary iron absorption is increased approximately fourfold once the iron stores are totally depleted.8 For iron to bind to DMT1, it must be soluble and in the ferrous state.Nonheme food iron as well as fortification iron added in the form of an iron salt or an elemental iron powder is solubilized in gastric juice primarily by the action of hydrochloric acid. All of this solubilized iron enters a common pool. Reduction of ferric iron is mediated by meal components such as ascorbic acid or by a putative diheme plasma membrane protein (Dcytb) that is present on duodenal...