A novel tool for distinguishing among root causes of iron overload or deficiency in humans has been discovered by US scientists.
Reporting their work in the journal Cell Metabolism, University of Utah researchers in Salt Lake City highlighted the fact that iron helps the body produce haemoglobin that enables red blood cells to carry oxygen, but too much iron could bind up and eventually damage organs.
The researchers said that the balance of iron in mammals is controlled by a liver-produced hormone called hepcidin and the iron transporting receptor ferroportin.
Hepcidin binds ferroportin to stimulate its break down, thereby lowering iron export. While too much hepcidin results in anaemia, too little of it disables the body to get rid of enough iron.
Now, the researchers have identified the critical hepcidin-binding domain (HBD) on ferroportin.
According to them, by placing that binding site on a bead, they now have a very specific method for detecting hepcidin levels in human blood.
"We've identified the hepcidin-binding site. It will allow the diagnosis of underlying inflammation to distinguish diseases of iron metabolism that stem from hepcidin versus those with other causes," said Jerry Kaplan, a university researcher.
He said that hepcidin was first known not for its effects on iron but for its antimicrobial action, and that the liver produces more of the hormone in response to inflammatory cytokines as a defence mechanism.