Published online in the journal Science this week, researchers discovered that the hormone hepcidin controls ferroportin, an iron-transporting molecule on the surface of specific cells that contain iron. Hepcidin signals ferroportin not to release iron into the blood stream.
Researchers realized that if there isn't enough hepcidin to regulate ferroportin, too much iron is taken up from the digestive system into the body, which can lead to hemochromatosis, a major genetic disorder affecting about a million people in the United States.
"For the first time we understand what happens in the disease hemochromatosis," said Dr. Tomas Ganz, Ph.D., M.D., one of the study's principal investigators and professor of medicine and pathology at the David Geffen School of Medicine at UCLA. "We knew that ferroportin is necessary to help release iron into the bloodstream, but didn't know that hepcidin directly regulates this activity."
Ganz adds that too much hepcidin present in the body -- which can occur in patients with infections or with inflammatory diseases such as rheumatoid arthritis or inflammatory bowel disease -- often results in not enough iron released into the blood stream causing chronic anemia.
"We have defined how the hormone hepcidin regulates the accumulation of iron by the body," says Jerry Kaplan, Ph.D., one of the study's principal authors and a professor of pathology and assistant vice president for basic science at the University of Utah Health Sciences Center. "This has implications for understanding both diseases that are caused by not enough iron and diseases that are caused by too much iron."