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Mice with hyperactive Wnt10b gene eat all they want, but have half the body fat of normal mice

ANN ARBOR, Mich. Genetically engineered mice, created at the University of Michigan Medical School, are living every dieter's dream. They eat unlimited amounts of high-fat mouse chow, but have about 50 percent less body fat than normal mice on a low-fat diet. And they show no signs of diabetes or other metabolic disorders, which are common in animals with too little fat.

But don't stock up on potato chips and ice cream just yet. The genetically altered mice are leaner than normal mice, but they also have some less-than-desirable characteristics such as underdeveloped mammary glands, an inability to generate body heat and skin that's twice as thick as normal.

All these changes appear to be caused by a protein called Wnt10b, which is present in artificially high amounts in fat tissue from the experimental mice. Wnt10b is one of a family of 19 related proteins. Wnts (pronounced "wints") regulate the complex changes that take place as an embryo grows. Part of this process is the development of fatty adipose tissue, which contains fat cells called adipocytes.

Ormond A. MacDougald, Ph.D., an associate professor of molecular and integrative physiology in the U-M Medical School, has spent years studying the effects of Wnt10b on the development of adipocytes. In August 2000, MacDougald and his colleagues published a paper in Science, showing that Wnt10b gene activity repressed fat cell development in tissue cultures.

Now, in the first study in living animals, MacDougald and Kenneth A. Longo, Ph.D, a U-M research fellow in physiology, have demonstrated that Wnt10b has the same effect on fatty tissue in mice.

"High levels of Wnt10b expression produced animals with 50 percent less body fat and fewer fat cells, regardless of whether the mice ate a high-fat or low-fat diet," MacDougald says.

Results of the U-M experiments were posted this month on the Journal of Biological Chemistry's "JBC Online" Web site (see URL at the end
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28-Jun-2004


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