'Fat switch' fights flab at the cellular level, Science authors report

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The discovery of a cellular "fat switch" -- described in the 11 August issue of the international journal, Science -- offers fundamental new information on obesity, a disease affecting nearly one-fourth of all adults in the United States alone.*

A protein called Wnt-10b apparently helps prevent flab by quieting two molecules known to crank out the genetic commands for fat formation, called "adipogenesis."

A simple animation, to be featured beginning 10 August on Science's STKE, the online Signal Transduction Knowledge Environment, shows pre-fat cells transforming. (Go to http://www.stke.org, then "Connections Map." Reporters: Call for earlier access to visuals.)

"Wnt signaling functions as a fat switch," explains doctoral candidate Sarah E. Ross of the University of Michigan School of Medicine, lead author of the Science article. "When it's on, fat-cell formation is repressed. When it's off, fat is initiated. Without this signal, muscle-cell precursors can even be reprogrammed to undergo adipogenesis, so that they turn to fat."

Such basic insights aren't likely to cure obesity in the near future. But, understanding the cellular events involved in adipogenesis "might suggest a series of targets to support the development of anti-obesity drugs, down the road," says Science coauthor Ormond A. MacDougald, an assistant professor of physiology at the university.

Secreted by cells, Wnt proteins regulate a variety of developmental processes through signal transduction, which occurs when biochemical signals move or "transduce" from cell to cell, or from a cell's surface to its interior, eventually influencing the expression of genes. Because signal

Contact: Ginger Pinholster
American Association for the Advancement of Science

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