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Originally published January 6 2006

Research yields new evidence about the significance of excessive iron levels in the body

by Mike Adams, the Health Ranger, NaturalNews Editor

Chu-Xia Deng, from the National Institute of Diabetes and Digestive and Kidney Diseases, has conducted research that demonstrates a link between a tumor suppressor gene located in the liver and the control over the level of dietary iron absorbed into the body.



A new study in the December Cell Metabolism reveals an unexpected connection between a tumor suppressor gene in the liver and the normally careful control over the amount of iron absorbed from the diet. The surprising finding demonstrates a critical role for the liver in iron metabolism. The discovery also suggests a new avenue for the treatment of hereditary hemochromatosis, an iron-overload disease that is one of the most common genetic disorders among Caucasians, according to researchers. Chu-Xia Deng, from the National Institute of Diabetes and Digestive and Kidney Diseases, and his colleagues report that mice lacking the SMAD4 gene in the liver only suffer from a toxic buildup of iron, particularly in their liver, kidneys, and pancreas--symptoms similar to those exhibited by humans with hemochromatosis. In other respects, the animals appeared remarkably normal, the researchers found. In the body, iron becomes part of hemoglobin, a molecule in the blood that transports oxygen from the lungs to all body tissues. Symptoms of hemochromatosis, the most common iron-overload disease, can include bronzed skin, enlarged liver, diabetes, and abnormalities of the pancreas and joints. A member of a critical cell signaling pathway known as the transforming growth factor � (TGF-�) superfamily, SMAD 4 plays many central roles in development. For example, mutations in the tumor suppressor gene are frequently detected in pancreatic cancer, colon cancer, and a common form of lung cancer called adenocarcinoma, Deng said. "Still, the mice were sick with apparent problems in their pancreas and other organs. Hepcidin secreted from the liver into the bloodstream is known to curb iron intake in the intestine and prevent the release of iron from cells in the blood, the researchers said. A lack of hepcidin has been associated with iron overload, whereas excess hepcidin results in iron-deficiency anemia in mice, the researchers said.


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