Intestinal iron-transport defect in the mouse with sex-linked anemia.

MANIS, JAMES. Intestinal iron-transport defect in the mouse with sex-linked anemia. Am. J. Physiol. 220(l) : 135-139. 1971.-Everted duodenal gut sacs prepared from mice with sex-linked anemia (sZa) have a defect in the serosal transfer step of the active transport mechanism for iron that prevents the establishment of concentration gradients across the intestine greater than 1.0. The defect is present in hemizygous males and homozygous females and is not anemia dependent. Heterozygous, carrier females have a partial serosal transfer defect, suggesting partial dominance of the sla gene. Duodenal loops in vivo also demonstrate the serosal transfer defect in sla mice, transferring decreased amounts of 5gFe from the intestine into the blood. More distal segments of sla intestine do not have enhanced iron transport to compensate for the defect in the duodenum. Calcium, galactose, and proline transport are normal in gut sacs prepared from sla mice. Stimuli resulting from increased iron needs, a low iron diet, or pregnancy fail to increase iron transport by duodenal gut sacs from sla mice in contrast to the marked increase in transport by sacs from normal mice.