The mechanisms for regulating absorption of Fe bis-glycine chelate and Fe-ascorbate in Caco-2 cells are similar
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Inorganic iron (Fe) absorption from the diet is controlled mainly in the intestinal tract where apical Fe uptake is inversely related to the Fe content in the enterocyte. Iron bis-glycine chelate is an iron compound that may be absorbed by a mechanism different from the regulated nonheme Fe pathway. Because Fe bis-glycine chelate is used increasingly as an Fe fortificant in foods, the critical question is whether this compound is a safe Fe supplement. We compared apical Fe uptake and transepithelial transport offered either as Fe-59 bis-glycine chelate or a Fe-59-ascorbate (Fe-AA) complex in Caco-2 cells, as a model of human intestinal epithelia, grown in different Fe concentrations in the media (0.5, 5 and 20 mumol/L Fe). Apical Fe uptake from Fe-59-AA and Fe-59 bis-glycine chelate did not differ nor did transepithelial transport rates. The rate of 59Fe uptake decreased with increasing intracellular Fe concentration (P < 0.001), an indication of a common absorption regulatory mechanism. We also evaluated the effect of an excess of Fe (100 μmol/L) provided as Fe bis-glycine chelate or Fe-AA on the incorporation of 1 μmol/L Fe-55-AA into Fe-replete Caco-2 cells. The inhibition of Fe bis-glycine chelate on the absorption of the extrinsic tag of Fe-55-AA (87.5%) did not differ from that of Fe added as Fe-AA (86.8%). These results suggest that Fe derived from Fe bis-glycine chelate and Fe-AA have similar regulatory absorption mechanisms.