CAMBRIDGE, Mass. Although cases of adult-onset diabetes have skyrocketed in the United States, researchers still don't know much about the biological processes that predispose so many people to the disease. But in research that will be published in the Oct. 16 issue of the journal Nature, scientists say they've found a protein that plays an essential role in regulating a cell's ability to absorb glucose, an important step toward gaining a better understanding of the underlying causes of diabetes.

Now that researchers know how this crucial protein reacts in normal cells, they can study how it functions in diabetic patients. The findings ultimately may lead to new drug targets for diabetes medications, says Harvey Lodish, a scientist at Whitehead Institute for Biomedical Research and co-author of the new study.

The researchers discovered the protein which they call TUG following a five-year search for molecules that control a glucose transporter named GLUT4, according to Jonathan Bogan, lead author on the paper and former scientist in both Lodish's laboratory and the Diabetes Unit at Massachusetts General Hospital.

"This discovery has all the attributes of being extremely important to understanding, and maybe treating, Type 2 diabetes," says Lodish.

Nearly 17 million Americans have Type 2 (adult-onset) diabetes, a disorder in which cells lose their ability to absorb glucose from the blood stream. This is different from Type 1 (juvenile onset) diabetes, in which the immune system attacks insulin-producing cells. Normally, when blood sugar levels rise, the pancreas secretes the hormone insulin, which travels through the blood and interacts with "receptors" on the surface of cells in muscle and fat, instructing the cells to absorb and store the excess glucose.

But in Type 2 diabetes, the cells become deaf to insulin's signals, a condition known as insulin resistance. "No one really knows what causes it," says Bogan, who
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Contact: David Cameron
newsroom@wi.mit.edu
617-258-5183
Whitehead Institute for Biomedical Research
15-Oct-2003

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