iron metabolism can lead to highly toxic free radicals [@Kell2009Iron]. Maintaining the delicate balance of iron requires robust cellular and systemic regulation since both iron deficiency and overload can cause cell death [@Hentze2004Balancing]. Recent research has lead to a much greater understanding of the mechanisms controlling iron metabolism and a global view of the interactions between iron-related components is beginning to emerge [@Dunn2007Iron; @Hower2009General].

The liver has been proposed to play a central role in the regulation of iron homeostasis [@Frazer2003Orchestration] through the action of the recently discovered hormone hepcidin [@Park2001Hepcidin]. Hepcidin is expressed predominantly in the liver [@Pigeon2001New] and distributed in the serum to control systemic iron metabolism. Hepcidin acts on ferroportin to induce its degradation. Ferroportin is the sole iron exporting protein in mammalian cells [@VanZandt2008Iron], therefore hepcidin expression reduces iron export into the serum from enterocytes, and reduces iron export from the liver. Intracellular iron metabolism is controlled by the action of iron response proteins (IRPs) [@Hentze1996Molecular]. IRPs post-transcriptionally regulate mRNAs encoding proteins involved in iron metabolism. IRPs combined with ferritin and the transferrin receptors (TfR) make up the center of cellular iron regulation. Ferritin is the iron-storage protein forming a hollow shell which counters the toxic 