BOSTON-March 26, 1999--A team of Harvard Medical School and Howard Hughes Medical Institute researchers have found that the transferrin cycle has a more limited role in iron transport than previously believed. The study, published in the April Nature Genetics, may eventually lead to improved diagnosis and treatment of iron metabolism disorders.
Led by Nancy Andrews, associate investigator of the Howard Hughes Medical Institute at Children's Hospital, Boston and a Harvard Medical School associate professor of pediatrics, the study is the latest in a recent flurry aimed toward a molecular understanding of how iron travels through the body.
Iron metabolism disorders--which include iron deficiency and iron overload diseases--afflict more than a billion people worldwide. Hemochromatosis, which is caused by an iron overload, is the most common genetic disorder among whites. Affecting up to 1 in 200 Caucasian Americans, hemochromatosis causes diabetes, impotence, arrhythmia and liver failure if untreated--and doctors often fail to diagnose it. Moreover, researchers are realizing that iron loading is more common among African Americans than previously thought.
Iron metabolism was intensely studied in the 1950s and '60s, when the physiology of this essential but potentially toxic metal was a research focus at hematology departments nationwide, Andrews says. The work slowed down because techniques to find key proteins in vivo were unavailable. However, the field picked up again when, in 1996, researchers discovered Hfe, the gene causing hemochromatosis and, in 1997, two groups at Harvard, including Andrews's lab, discovered that another gene, Nramp2, is responsible for transporting dietary iron into the cells lining the small intestine.
Andrews began her research on iron by analyzing a legacy of the old
work: strains of mice dating back to the 1920s and '30s that had defects so
carefully described by hematologists that she co
Contact: Bill Schaller
Harvard Medical School