Studies on the control of iron uptake by rabbit small intestine.

1. Whole-body retention in vivo and uptake of 59Fe-labelled ascorbate and nitrilotriacetate chelates by intestinal slices in vitro were determined in groups of normal control rabbits and rabbits with experimentally-induced Fe deficiency. 2. Over-all absorption as measured by retention of doses of either chelate was greatly increased in conditions of Fe deficiency. 3. Intestinal Fe uptake in vitro was inhibited up to 77% in the presence of 2,4-dinitrophenol and sodium fluoride. Initial rates showed saturation within the concentration range 18-450 mumol/l, suggesting that uptake was brought about by an active transport process. 4. When studied at chelate concentrations of 450 mumol/l, significant regional differences in uptake rates were observed. Uptake in duodenal slices was increased when compared with slices from jejunum and ileum. 5. Fe uptake from ferric and ferrous chelates was greatly enhanced in Fe deficiency. This was chiefly due to increases in uptake by slices from the duodenum, but uptake into slices of distal intestine was also stimulated. 6. Kinetic analysis of Fe uptake by duodenal slices from animals rendered Fe deficient by diet or repeated bleeding indicated in both groups an increased apparent maximum velocity (Vmax) for influx of Fe without significant changes in apparent affinity for Fe. 7. The experiments provide further insight into the nature and regional distribution of transport of Fe into the intestine and suggest, in the rabbit, that important control of Fe absorption may be exerted by an active process operating at this initial entry step.