Cells in the intestine (A) absorb iron that is passed along to the bloodstream (B). Previously it was thought that the Hfe mutation found in Hemochromatosis acted to change the behaviour of these cells. The latest research shows that the mutation seemsto act primarily in the liver.
Researchers at EMBL and Harvard gain new insights into hemochromatosis
Like most nutrients, iron is good for people – in the right doses. When the body has enough iron, our cells stop absorbing it from food; if there is too little, they absorb more. This system breaks down in the most common inherited disease in the Western world: hemochromatosis, which affects about one in every 250 people and is often fatal if it is not recognized and treated. Now researchers at the European Molecular Biology Laboratory in Heidelberg (EMBL) and Harvard Medical School (U.S.) have linked the response of a gene in the liver to the disease. The study, which appears in the current issue of Nature Genetics, is changing our understanding of how hemochromatosis develops.
"Untreated iron overload can result in liver cancer, heart disease, or other fatal conditions," says Martina Muckenthaler, a staff scientist at EMBL in the research group of Matthias Hentze. "The mutation that causes the disease was thought to have its major effects in the intestine, where cells absorb iron from food. Our current study has changed that picture."
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