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Mouse, stripped of a key gene, resists diabetes

MADISON - An engineered mouse, already known to be immune to the weight gain ramifications of a high-calorie, high-fat diet, now seems able to resist the onset of diabetes.

The mouse, stripped of a gene known as SCD-1, is apparently impervious to the negative effects of the type of diet that, for many people, has significant health and social consequences.

"We think this animal model may be protected against diabetes," says James Ntambi, a University of Wisconsin-Madison professor of biochemistry and Steenbock professor of nutrition, and the senior author of a report describing the remarkable mouse in this week's (Sept. 1) online editions of the Proceedings of the National Academy of Sciences (PNAS).

The new finding is important because it provides critical genetic and biochemical clues to diet, obesity and the onset of a disease that affects as much as 6 percent of the U.S. population.

Type II diabetes, which accounts for about 90 percent of the incidence of diabetes in the United States, is a chronic disease caused by a problem in the way the body makes or uses insulin. Insulin is a hormone secreted by the pancreas that, under healthy circumstances, plays an essential role in moving glucose from blood to cells where the sugar's energy is expended.

In many instances, obesity and diabetes go hand in hand. Between 75 and 80 percent of people with type II diabetes are obese, although the disease can also develop in lean people, especially the elderly.

The discovery of a gene that seems to exercise significant influence over both weight gain and glucose regulation promises a potentially significant window into both conditions and their relationship. The gene makes an enzyme called SCD. It affects the production of fatty acids, and because humans have SCD-1 equivalents, the new finding helps explain why some people, who may lack the gene, remain lean and diabetes free, despite a rich, fatty diet.

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Contact: James Ntambi
ntambi@biochem.wisc.edu
608-265-3700
University of Wisconsin-Madison
2-Sep-2003


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