Key to regulating iron metabolism

SAN DIEGO, June 21 (UPI) -- San Diego researchers have determined a key mechanism regarding the body's iron metabolism regulation that may help treat anemia.

A collaborative effort between the laboratories of Randall Johnson, the University of California San Diego and Dr. Victor Nizet, UCSD School of Medicine, discovered that a protein known as hypoxia-inducible transcription factor, or HIF, is critical in orchestrating the proper hepcidin response in the liver.

Hepcidin hormone is a peptide -- small protein -- that is synthesized in the liver and regulates the levels of iron in the body. It prevents the body from absorbing more iron than is needed from food or supplements, and blocks the export of iron from cells.

Patients with cancer, chronic inflammatory diseases or infections often develop high levels of hepcidin, which reduces the amount of iron available to support the production of new red blood cells, resulting in anemia.

The finding suggests that new drug treatment strategies to boost HIF or inhibit vHL -- von-Hippel Lindau factor, a protein that controls HIF levels -- could reverse the abnormally high hepcidin levels seen in the anemia that affects the majority of patients suffering from chronic infections or inflammatory disease, according to the study published in a special supplement in the American Journal of Nursing.