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1 Genetics and Complex Diseases, Harvard School of Public Health, Boston, Massachusetts, United States
2 Environmental Health, Harvard School of Public Health, Boston, Massachusetts, United States
3 Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, United States
* To whom correspondence should be addressed. E-mail: wessling{at}hsph.harvard.edu.
Divalent Metal Transporter-1 (DMT1) mediates dietary non-heme iron absorption. Belgrade (b) rats have defective iron metabolism due to a mutation in the DMT1 gene. To examine the role of DMT1 in neonatal iron assimilation, b/b and b/+ pups were cross-fostered to F344 Fischer dams injected with 59FeCl3 twice weekly during lactation. Tissue distribution of the radioisotope in the pups was determined at weaning (day 21). The b/b pups had blood 59Fe levels significantly lower than b/+ controls, but significantly higher 59Fe tissue levels in heart, bone marrow, skeletal muscle, kidney, liver, spleen, stomach, and intestines. To study the pharmacokinetics of non-heme iron absorption at the time of weaning, 59FeCl3 was administered to 21-d-old b/b and b/+ rats by intragastric gavage. Blood 59Fe levels measured 5 min to 4 h post-gavage were significantly lower in b/b rats, consistent with impaired DMT1 function in intestinal iron absorption. Tissue 59Fe levels were also lower in b/b rats post-gavage. Combined, these data suggest that DMT1 function is not essential for iron assimilation from milk during early development in the rat.
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