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Rodents lacking gene feel the burn: study finds mutated mice use energy instead of storing fat.

Mice with a mutation in an immune system gene don't get fat, they burn it.

A gene that helps regulate inflammation also stops fat cells from wasting energy. When the gene, I kappa B kinase epsilon or IKK[epsilon], is missing, mice turn a high-fat diet into heat instead of body fat, a study in the Sept. 4 Cell shows.

If the gene works the same way in humans as in mice, it could be a new target for antiobesity drugs.

Scientists know that low-level inflammation produced by obesity can trigget type 2 diabetes, but the details are unclear, says Alan Saltiel of the University of Michigan in AnnArbor. In the new study, Saltiel and his colleagues found that in mice fed a high-fat diet, levels of the IKK[epsilon] protein were elevated in the liver and fat tissue, compared with mice on a regular chow diet. IKK[epsilon] is involved in regulating inflammation, and the researchers thought the protein might be the link between diet and diabetes.

"What I expected was that if we knocked out this gene we'd get rid of the link between obesity and diabetes." by eliminating inflammation, Saltiel says. He didn't suspect the connection would be severed further up the chain- preventing mice from getting obese to begin with.

Mice lacking the gene increase production of uncoupling protein, or UCP1, an energy-burning protein. It is found in mitochondria, the cell's power plants. Excess UCP1 causes fat cells to burn more energy and release it as heat.

Normally, IKK[epsilon] "keeps the brakes on the expression of UCP1 in white fat," Saltiel says. "When we knocked out IKK[epsilon], we released the brakes."

After three months on a high-fat diet, the mice with the mutation gained an average of 12 grams, while normal mice gained about 20 grams. Although the mutant mice still gained some weight, the researchers say that it wasn't enough to trigger the inflammation and diabetes associated with obesity. When fed a normal diet. both types of mice weighed about 32 grams on average.

Removing IKK[epsilon] clearly changes the mice's energy balance, says C. Ronald Kahn of Harvard's Joslin Diabetes Center, but the mechanism still isn't understood. He suspects that the mutant mice have more energy-burning brown fat cells, rich in UCP1, mixed in with white fat.


Previous studies have shown that mice lacking the immune gene are more susceptible to deadly viral infections. But Saltiel says that potential drugs inhibiting IKK[epsilon] to fight obesity probably wouldn't turn the gene off completely, leaving enough activity to combat infections. White blood cells from the mutant mice in the new study responded normally to a substance designed to mimic a bacterial infection.

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Title Annotation:Body & Brain
Author:Saey, Tina Hesman
Publication:Science News
Geographic Code:1USA
Date:Sep 26, 2009
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