Published online Feb 6, 2017. doi: 10.5315/wjh.v6.i1.17
Peer-review started: September 1, 2016
First decision: October 26, 2016
Revised: November 18, 2016
Accepted: December 16, 2016
Article in press: December 19, 2016
Published online: February 6, 2017
To investigat the influence of hemochromatosis gene (Hfe) mutation on 59Fe labelled duodenal heme absorption in mice.
Heme absorption was measured in Hfe wild type and Hfe(-/-) mice by the duodenal tied loop and by oral gavage methods. The mRNA expression of heme oxygenase (HO-1), Abcg2 and Flvcr1 genes and levels were determined by quantitative polymerase chain reaction.
Heme absorption was significantly increased in homozygous Hfe(-/-) mice despite significant hepatic and splenic iron overload. While duodenal HO-1 mRNA was highly expressed in the wild type and Hfe(-/-) heme-treated group following 24 h heme administration, Flvcr1a mRNA decreased. However, Abcg2 mRNA expression levels in duodenum remained unchanged.
Heme absorption was enhanced in Hfe(-/-) mice from both duodenal tied-loop segments and by oral gavage methods. HO-1 mRNA levels were enhanced in mice duodenum after 24 h of heme feeding and may account for enhanced heme absorption in Hfe(-/-) mice. Implications for dietary recommendations on heme intake by Hfe subjects to modulate iron loading are important clinical considerations.
Core tip: These results indicate that loss of hemochromatosis gene (Hfe) protein results in increased dietary heme iron absorption that further contributes to the iron loading of the liver and other tissues of mice. Enhanced heme iron intake by homozygous Hfe subjects may contribute to body iron overload and early manifestation of phenotypic traits. This may have implications for dietary recommendations on heme intake by hemochromatosis subjects to avert tissue iron loading.