Maintenance of iron balance is essential for humans and requires the coordinate 
regulation of iron transport into plasma from dietary sources in the duodenum, 
from recycled senescent red cells in macrophages, and from storage in 
hepatocytes. Hepcidin, a recently identified antimicrobial peptide produced in 
the liver, has been shown to play a central role in the homeostatic regulation 
of iron absorption and distribution [1]. It is a negative regulator of iron 
absorption in the small intestine and of iron release from macrophages engaged 
in the recycling of iron senescent erythrocytes [2]. The human hepcidin gene 
contains three exons that encode a 72-aa precursor (pro-hepcidin) with a 
characteristic furin cleavage site immediately N-terminal to the 25-aa major 
hepcidin species found in plasma and urine [3]. Recently, hepcidin has been 
shown to regulate iron homeostasis by interaction with ferroportin, an iron 
cellular exporter highly expressed in absorptive enterocytes, macrophages, 
hepatocytes, and placental cells [4].