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A new target for control of obesity

La Jolla, CA. A team of researchers led by The Burnham Institute's Gen-Sheng Feng, Ph.D. has discovered that a protein called Shp2 plays a critical role in obesity. Published on November 9th in Proceedings of the National Academy of Sciences, these results show that Shp2 has potential of becoming a novel pharmaceutical target for treatment of individuals suffering obesity and leptin resistance.

In 2003, the World Health Organization identified obesity as a growing global threat affecting more than 300 million people worldwide. Although it is commonly believed that obese individuals can overcome their condition by simply eating less and exercising more, compelling scientific data suggest that the heritability of obesity is greater than breast cancer, heart disease, or schizophrenia. Morbid obesity is considered as the disease of the twenty-first century, with the affected individuals at higher risk for diabetes, heart disease, hypertension and cancer, collectively known as metabolic syndrome.

Shp2, a Src homology 2-containing tyrosine phosphatase, was discovered by Dr. Feng and others over a decade ago. It is present in each cell type in the body and is implicated in a variety of growth factor or cytokine pathways present in these cells.

The physiological function of Shp2 is largely unknown. Whether it is active in multiple pathways or focused on a single pathway remains to be seen. In recent years, in vitro experiments suggest that Shp2 plays a role in regulating the protein leptin. Leptin, produced in fat cells, is a hormone that regulates body weight, metabolism, and reproduction. The primary action site for leptin is within the hypothalamus, located in the forebrain.

Dr. Feng and his colleagues took the investigation to the next level by looking at the role of Shp-2 in live mice. They bred a special kind of mouse in which the elimination of Shp-2 was confined to the mouse's forebrain by using a highly ad
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Contact: Nancy Beddingfield
nbeddingfield@burnham.org
848-449-9940
Burnham Institute
8-Nov-2004


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