Binding iron (Fe) to the 1-25 caseinophosphopeptide obtained from enzyme hydrolysis of beta casein (beta CPP) improves Fe bioavailability in the rat. To assess the mechanisms involved in its absorption, a perfused, vascularized duodenal rat loop model was used in controls and in Fe-deficient (bleeding of 25% blood volume) rats. Inhibitors of oxidative phosphorylation [2-4 dinitrophenol (DNP)] and/or of endocytosis [phenylarsine oxide (PAO)] were added to the perfusion solution containing 50 microM Fe as beta CPP bound Fe (Fe-beta CPP) or gluconate (Fe Gluc). Fe-beta CPP enhanced Fe uptake, reduced mucosal storage, and improved net absorption both in controls and in deficient animals. DNP reduced uptake, mucosal storage, and net absorption by the same percentage in Fe-beta CPP and Fe Gluc perfused rats in both control and Fe-deficient animals. PAO decreased uptake, mucosal storage, and net absorption of Fe-beta CPP but not of Fe Gluc. At the end of the experiment Fe serum levels were increased only in Fe Gluc animals. These results confirm the improved bioavailability of beta CPP bound Fe. They suggest that at least part of its absorption can occur by a different pathway than usual Fe salts. Fe-beta CPP can be taken up by endocytosis and absorbed bound to amino acids or peptides.

Summary -Digestive absorption of iron bound to the 1-25 caseinophosphopeptide of~-casein. We investigated the digestive absorption of iron using an isolated, perfused rat intestinalloop. Iron bound to the 1-25 caseinophosphopeptide of~-casein (~-CN (1-25» was compared to iron gluconate. Half of the animals were bled to induce an acute iron deficiency, which enhances iron absorption; the protective effect of~-CN (1-25) against the calcium inhibition of iron absorption was tested as weIl. In the control or anemie groups, iron disappearance from digestive lumen was higher in thẽ -CN (1-25) than in the gluconate group. In control animaIs the amount of iron stored was lower iñ -CN (1-25) animaIs than in animaIs perfused with gluconate, while both groups of anemie animaIs also displayed lower enterocyte retenti on than control animaIs. As a result, the net iron absorption was higher in animaIs perfused with~-CN (1-25) than with gluconate, whether the animaIs were iron depleted or not. Addition of calcium to the perfused solution decreased iron absorption, however, this decrease was significantly reduced in~-CN (1-25) groups. The increased solubility of iron bound to~-CN (1-25) could explain these results, in association with enhancement of the mucosal transfer of iron taken up by the enterocyte.Résumé -L'absorption digestive du fer lié au 1-25 caséinophosphopeptide issu de la~-caséine (~-CN [1-25]) a été comparée à celle du gluconate de fer par le modèle d'intestin perfusé isolé, vascularisé de rat, à l'état basal et dans deux conditions connues pour augmenter l'absorption du fer (saignée) ou l'inhiber (présence de calcium). Chez l'animal normal ou après saignée, la disparition du fer de la lumière intestinale du groupe~-CN (1-25) est supérieure à celle du groupe gluconate. Chez l'animal normal, la rétention entérocytaire du fer est plus faible dans le groupe~-CN (1-25) que * Correspondence and reprints 434 lM Peres et al dans le groupe gluconate. Après saignée, elle est semblable dans les deux groupes et est significativement inférieure à celle des animaux normaux. En conséquence, chez les animaux normaux ou anémiques, l'absorption nette est plus élevée dans les groupes~-CN (1-25) que dans les groupes perfusés avec du gluconate. La fixation du fer au~-CN (1-25) limite significativement l'effet inhibiteur du calcium sur son absorption, chez l'animal contrôle et anémique. Ces résultats semblent dus à la protection intraluminale apportée au fer par sa liaison au~-CN (1-25) soluble, associée à une modification du transport entérocytaire du fer capté.fer / absorption digestive / caséinophosphopeptide~-CN

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