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Chewing up a key regulator of fat synthesis keeps mice lean despite a high-fat diet

only during fasting, when ACC should be turned off. Heredia and co-first author Ling Qi, Ph.D., reasoned that keeping the TRB3 pathway artificially "on" during both fasting and feeding might melt away fat depots.

And that's exactly what happened. Mice genetically engineered to express permanently elevated levels of TRB3 protein in fat tissue were 10-20 percent skinnier than normal mice. "Even when we put them on a high-fat diet, these mice just didn't gain any weight," says Qi. "Their physical activity was the same, but they were constantly burning fat."

All this is good news for the fight against obesity and the disorders characterized by insulin-resistance known as "metabolic syndrome." Most people with insulin resistance will develop type 2 diabetes within 10 years, unless they lose 5 to 7 percent of their body weight--about 10 to 15 pounds for someone weighing 200 pounds. Defining how molecules regulating fat storage interact could lead to novel measures to curb obesity.

Further evidence linking TRB3 to disease comes from recent findings from a team of Italian scientists who report that mutations in the human TRB3 gene are associated with several insulin resistance-related health problems, such as high insulin levels, high cholesterol, and cardiovascular disease.

Achieving a desired physiological outcome by manipulating basic biochemistry was clearly satisfying for Montminy. "What really made this an interesting story is that the molecular mechanism and the biology intersected since we were able to explain how TRB3 made the mice lean," he reflects. "That doesn't happen very often."

Additional contributors to this study included assistant professor Robert Screaton, Ph.D., formerly at the Salk, now at Children's Hospital of Eastern Ontario; Judith Y. Altarejos, Ph.D., Naomi Goebel, Michael Nelson, Ph.D., professor Ronald M. Evans, Ph.D., all at the Salk Institute; Sherry Niessen, Ian X. MacLeod, and Professor John Yates, P
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Source:Salk Institute


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