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Insulin Resistance And Obesity Avoided In Genetically Modified Mice, As Reported In Science

Washington D.C. - A team of Canadian scientists has identified a potentially useful target for drugs to treat type II diabetes and obesity. In the scientists' experiments, genetically engineered mice lacking a specific enzyme were able to resist weight gain and to avoid the decreased sensitivity to insulin that characterizes type II diabetes, even when fed an extremely high calorie, high fat diet. The results are reported in the 5 March issue of Science.

The finding raises hopes that researchers might someday design a drug for humans that mimics these effects by targeting the same enzyme. "It will certainly take some time to find a compound useful for humans based on our mouse model, but it has the possibility of being a really significant drug if it works," said Brian Kennedy of the Merck Frosst Center for Therapeutic Research in Pointe Claire-Dorval, Quebec, Canada, who was a member of the research team.

In 1995, there were 35 million cases of type II diabetes, or "non-insulin-dependent diabetes," worldwide, according to the World Health Organization, which predicts that the number will radically increase over the next 25 years. Type II diabetes usually develops gradually in people over 40, and overweight people are at particularly high risk for the disease. Diabetes occurs when the body's cells are unable to absorb enough blood sugar, or glucose, into their cells. This lack of cellular "fuel" and the high levels of glucose in the blood stream cause weight loss, fatigue, and a variety of long-term complications.

To store and use glucose, cells need assistance from the hormone insulin, which controls a complex series of steps to remove glucose from the bloodstream and sequester it in the cells. This set of steps is called the insulin "signal." People with type I diabetes (the more severe and early-onset form of the disease) do not produce insulin at all and must
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Contact: Gabriel Paal
gpaal@aaas.org
202-326-6421
American Association for the Advancement of Science
5-Mar-1999


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