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Am J Physiol Gastrointest Liver Physiol 289: G981-G986, 2005; doi:10.1152/ajpgi.00363.2005
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THEMES

Iron Imports. II. Iron uptake at the apical membrane in the intestine

Bryan Mackenzie1 and Michael D. Garrick2

1Department of Molecular and Cellular Physiology, University of Cincinnati College of Medicine, Cincinnati, Ohio; and 2Departments of Biochemistry and Pediatrics, State University of New York, Buffalo, New York

How does iron enter enterocytes? Ablating SLC11A2, the gene for the divalent metal ion transporter DMT1, supports evidence from the Belgrade rat and mk mouse models establishing DMT1 as the primary mechanism serving apical uptake of nonheme iron. DMT1 harnesses the energy from the proton electrochemical potential gradient to drive active transport of Fe2+ (and perhaps Mn2+ and other metal ions) into enterocytes. Fe(III) must first be reduced by ascorbic acid and surface ferrireductases. Among these is duodenal cytochrome B (DcytB), but lack of an obvious phenotype in DcytB (Cybrd1) knockout mice suggests ferrireductase redundancy. Our understanding of heme absorption has lagged, but the time is ripe for gains.

anemia; duodenal cytochrome B; divalent metal ion transporter; ferroportin; hemochromatosis; iron absorption; Nramp2; SLC11A2


Address for reprint requests and other correspondence: B. Mackenzie, Dept. of Molecular and Cellular Physiology, Univ. of Cincinnati College of Medicine, PO Box 670576, Cincinnati, OH 45267-0576 (e-mail: bryan.mackenzie{at}uc.edu)




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