Blood, 15 April 2003, Vol. 101, No. 8, pp. 3316-3318
RED CELLS
Brief report
Duodenal nonheme iron content correlates with iron stores in
mice, but the relationship is altered by Hfe gene
knock-out
Robert J. Simpson,
Edward S. Debnam,
Abas H. Laftah,
Nita Solanky,
Nick Beaumont,
Seiamak Bahram,
Klaus Schümann, and
S. Kaila S. Srai
From the Department of Life Sciences, King's College
London, England; Departments of Physiology and Molecular
Biology, Royal Free and University College School of Medicine, London,
England; INSERM-CreS, Centre de Recherche d'Immunologie
et d'Hématologie, Strasbourg, France; and
Walther-Straub-Institut für Pharmakologie und Toxikologie,
Ludwig-Maximilians-Universität, München,
Germany.
Hereditary hemochromatosis is a common iron-loading disorder found
in populations of European descent. It has been proposed that mutations
causing loss of function of HFE gene result in reduced iron
incorporation into immature duodenal crypt cells. These cells then
overexpress genes for iron absorption, leading to inappropriate
cellular iron balance, a persistent iron deficiency of the duodenal
mucosa, and increased iron absorption. The objective was to measure
duodenal iron content in Hfe knock-out mice to test whether
the mutation causes a persistent decrease in enterocyte iron
concentration. In both normal and Hfe knock-out mice,
duodenal nonheme iron content was found to correlate with liver iron
stores (P < .001, r = 0.643 and 0.551, respectively), and this effect did not depend on dietary iron levels.
However, duodenal iron content was reduced in Hfe knock-out
mice for any given content of liver iron stores
(P < .001).
