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1 Department of Nutrition, University of California, Davis, CA, USA
2 Department of Internal Medicine, University of California, Davis, CA, USA
3 Department of Pharmacology and Toxicology, Uppsala Biomedical Center, Uppsala, Sweden
4 Department of Nutrition, University of California, Davis, CA, USA; Department of Internal Medicine, University of California, Davis, CA, USA
* To whom correspondence should be addressed. E-mail: bllonnerdal{at}ucdavis.edu.
Two iron transporters, divalent metal transporter1 (DMT1) and ferroportin1 (FPN1) have been identified; however, their role during infancy is unknown. We investigated DMT1, FPN1, ferritin and transferrin receptor expression, iron absorption and tissue iron in iron-deficient rat pups, iron-deficient rat pups given iron supplements and controls during early infancy (d10) and late infancy (d20). With iron deficiency, DMT1 was unchanged and FPN1 was decreased (-80%) at d10. Body iron uptake, mucosal iron retention and total iron absorption were unchanged. At d20 DMT1 increased 4-fold and FPN1 increased 8-fold in the low Fe group compared to controls. Body iron uptake and total iron absorption were increased and mucosal iron retention was decreased with iron deficiency. Iron supplementation normalized expression levels of the transporters, body iron uptake, mucosal iron retention and total iron absorption of the low Fe group to those of controls at d20. In summary, the molecular mechanisms regulating iron absorption during early infancy differ from late infancy when they are similar to adult animals, indicating developmental regulation of iron absorption.
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