Researchers have identified an enzyme that could hold the key to reducing obesity. Mice genetically manipulated to be deficient in the enzyme acetyl-CoA carboxylase 2 (ACC2), they discovered, can eat up to 40 percent more than normal mice and still weigh 10 to 15 percent less. The findings appear today in the journal Science.

Salih Wakil of the Baylor College of Medicine and his colleagues first identified the enzyme in 1989. Their new research, however, demonstrates its role in transporting fatty acids to the cell's energy-producing organelles or mitochondria. Using so-called "knockout mice," the team discovered that animals lacking the enzyme adapted to their condition quite favorably. "The mice genetically engineered to lack ACC2 seem very happy, [and] live and breed well," Wakil notes. The major difference, it seems, is that they weigh less and accumulate less fat than do the normal animals.

"This enzyme ACC2 could be a target for generating drugs that could regulate the burning of fat," Wakil remarks. "It could be important in the regulation of obesity, treatment of diabetes and eventually even the utilization and accumulation of fat, which could affect diseases such as atherosclerosis."