Iron Homeostasis and Nutritional Iron Deficiency

Nonheme food ferritin (FTN) iron minerals, nonheme iron complexes, and heme Iron contribute to the balance between food iron absorption and body iron homeostasis. Iron absorption depends on membrane trarsporter proteins DMT1, PCP/HCP1, ferroportin (FPN). TRF2, and matriptase 2. Mutations in DMT1 and matnptase-2 cause iron deficiency; mutatons in FPN, HFE, and TRF2 cause iron excess. Intracellular iron homeostasis depends on coordinated regulation of iron trafficking and storage proteins encoded in iron responsive element (IRE)-mRNA. The noncoding IRE-rnRNA structures bind protein repressors, iRP1 or 2, during iron deficiency. Integration of the IRE-HNA in translat or regulators (near the cap) or turnover elements (after the coding region) increases iron uptake (DMT/TRF1) or decreases iron storage/efflux (FTN/FPN) when IRP binds. An antioxidant response element in FTN DNA binds Bach 1, a heme-sensitive transcrption factor that coordinates expression among ant oxidant response proteins like FIN, thioredoxin reductase, and quinone reductase. FTN, an antioxidant because Fe2- and O-2 (reactive oxygen species generators) are consumed to make iron mineral, is also a nutritional iron concentrate that is an efficiently absorbed, nonheme source of iron from whole legumes. FTN protein cages contain thousands of mineralized iron atoms and enter cells by receptor-mediated endocytosis, art absorption mechanism distinct from transport of rorheme iron salts (ferrous sulfate), iron chelators (ferric-EDTA), or heme. Recognition of 2 nutritional nonheme iron sources, small and large (FTN), will aid the solution of iron deficiency, a major public health problem, and the development of new pole es on iron nutrition. J. Nutr. 141: 724S-728S, 2011.