1. A standardized decompensation and recompensation of iron homeostasis has been produced by a change-over from normal to iron deficiency and back. 2. Under these conditions the 59Fe uptake into transferrin and ferritin of the mucosal "cytosol" and SDS treated "membrane" fraction has been measured together with the 59Fe amount transferred into the body. 3. The increase of the intestinal 59Fe absorption due to a progressive iron deficiency is associated with an increase of the 59Fe uptake into the mucosal transferrin of the "cytosol" and the "membrane" fraction; the reverse is observed with regard to mucosal ferritin. 4. Three days after the re-establishment of normal conditions the 59Fe absorption was lowered to normal values, while the 59Fe uptake into mucosal ferritin achieved again normally high values. 5. The high apparent rate of absorption in iron deficient animals decreased during the last 50 min after injection of the 59Fe labelled test dose. The 59Fe content in the ferritin fraction increased simultaneously, whereas the 59Fe content in the transferrin fraction remained the same. 6. The conclusion is drawn that the intestinal iron absorption is regulated by both mucosal iron binding proteins. Mucosal transferrin is responsible for the increase of absorption in iron deficiency while mucosal ferritin is responsible for the inhibition of iron absorption when the iron homeostasis recompensats.
1. The chromatographic elution patterns on Sepharose 6B of the supernatant from mucosal homogenates prepared 10 min after administration of copper into duodenal segments in vivo, indicate that copper is bound preferentially in the fraction of mucosal transferrin. 2. In iron deficiency the amount of 64Cu-copper taken up into the duodenal mucosa is more than two times higher and the amount bound to proteins of the supernatant is also increased to approximately the same degree whereas the amount transferred into the body is diminished to one fourth. 3. In the iron deficient group 64Cu-copper was also bound to a fraction which contains probably metallothionein. 4. The distribution of copper in the supernatant was changed due to a simultaneous administration of iron; the amount of copper bound in the transferrin fraction decreased in favor of the metallothionein fraction and another copper binding fraction was eluted between the transferrin and the metallothionein fraction. 5. Copper in a tenfold molar excess inhibited the iron absorption; simultaneously, the iron bound in the iron binding fractions of the supernatant was remarkably diminished. 6. The results suggest that the affinity of copper to two mucosal iron binding proteins, transferrin and metallothionein, is at least partly responsible for the inhibitory effect of copper on iron absorption in iron deficiency.
The uptake of iron from a tied off jejunal segment into the body after the injection of a 59Fe labeled test dose was decreased after the administration of endotoxin by about 80% in both normal and iron deficient animals.--In the iron deficient group the distribution of 59Fe in the cytosol fraction of jejunal mucosa between transferrin and ferritin was determined chromatographically; the amount of 59Fe in the ferritin fraction increased remarkably after the endotoxin treatment and the ratio of both was changed in favor of ferritin.--It is hypothesized that the association of the diversion of iron to the mucosal ferritin with the decrease of the transport of iron into the blood caused by endotoxin might be the consequence of abnormal oxidations in the mucosa measured by others in liver tissue.
The effect of vitamin C or carotene either in the authentic form or naturally occurring as in orange, parsley and pepper juices on calcium absorption was studied. Results obtained revealed that ascorbic acid, orange and pepper juices enhanced intestinal calcium absorption. Carotene and parsley proved to be without effect.
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