Defective iron uptake by the duodenum of belgrade rats fed diets of
different iron contents.
Oates, Phillip S., and Evan H. Morgan.
Department of Physiology, The University of Western Australia,
Nedlands 6907, Western Australia
APStracts 2:0246G, 1995.
Homozygous Belgrade rats have an inherited hypochromic, microcytic
anemia which is due to impaired iron (Fe) transport into immature red
blood cells. There is also evidence for abnormal Fe transport in
other tissues such as the intestine. This study was aimed at
investigating the intestinal defect in rats which had been fed diets
which are normal, low or high in iron for 12 days. The duodenal
uptake, transfer and absorption of Fe (III)-nitrilotriacetate and Fe
(II)-ascorbate were studied using in vivo, tied off, gut sacs in
genetically normal rats and in heterozygous or homozygous Belgrade
rats. In normal and heterozygous Belgrade rats the handling of Fe
(III) and Fe (II) was similar; uptake, transfer and absorption of Fe
(III) and Fe (II) changed inversely with the Fe content of the diet.
In contrast, in homozygous Belgrade rats the uptake of both Fe (III)
and Fe (II) was markedly reduced and absorption of Fe (III) did not
change with the feeding of an iron deficient diet. Since absorption
of Fe (II) was similar to Fe (III), there is no evidence that the
defect in Fe absorption is due to failure of a mechanism for
reduction of Fe (III). The lowered uptake of Fe (III) and Fe (II) in
homozygous Belgrade rats probably involves a defective iron carrier
associated with the microvillous membrane of the duodenum.
Received 22 June 1995; accepted in final form 16 November 1995.
APS Manuscript Number G268-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95