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Research Article Free access | 10.1172/JCI106807
Department of Internal Medicine, The University of Texas (Southwestern) Medical School, Dallas, Texas 75235
Veterans Administration Hospital, Dallas, Texas 75216
Find articles by Sheehan, R. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, The University of Texas (Southwestern) Medical School, Dallas, Texas 75235
Veterans Administration Hospital, Dallas, Texas 75216
Find articles by Frenkel, E. in: JCI | PubMed | Google Scholar
Published February 1, 1972 - More info
Gastrointestinal mucosal factors controlling rates of iron absorption were studied utilizing an in vivo closed duodenal loop technique. Cellular distribution of newly absorbed radioiron was identified by molecular sieve and iron-exchange chromatography of the mucosal cell supernate. In the normal animal, iron rapidly appeared in ferritin, and this fraction accounted for greater than 90% of mucosal supernatant radioactivity after 60 min absorption time. The nonferritin radioiron appeared to be unbound iron salts. In the presence of increased iron absorption induced by iron depletion or hemolysis, the major difference from the normal distribution pattern was an increase in the proportion and quantity of the free iron salts. Incorporation of newly absorbed iron into ferritin did not correlate with the rate of iron absorption. No evidence was found for a specific soluble iron-chelating molecule within the mucosal cell. The nonheme iron content of the mucosal supernates from iron-deficient and hemolyzing animals were significantly lower than in the normal animal.
The data are consistent with hypotheses which suggest that iron absorption rates may be controlled in part by the rate of initial iron uptake by the mucosal cell and that a membrane transport mechanism exists which is modulated by the nonheme iron content of the mucosal cell or some portion thereof.