Designer Mice Eat More, Weigh Less

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"Eat more, weigh less"--it sounds like the advertising slogan of a weight loss program. But it is a reality for a certain type of genetically engineered mouse, providing tantalizing possibilities for treating obese humans. Obesity is responsible for the deaths of 280,000 adult Americans each year, making it a leading cause of preventable death in the United States. The total cost of treating overweight and obese individuals approaches $100 billion annually. (1) Excess body weight and obesity also increase the risk of a range of diseases, including diabetes, heart disease, stroke, and various cancers.

For more than 10 years, Dr. Salih Wakil of Baylor College of Medicine and his coworkers have studied an enzyme called acetyl-CoA carboxylase 2, or ACC2, which governs the body's ability to burn fat. The researchers recently discovered that mice designed to lack this enzyme eat 20 to 30 percent more food, and yet accumulate less fat and weigh about 10 percent less than normal mice. Best of all, the engineered mice are otherwise normal--"[ they] seem very happy, live and breed well," says Dr. Wakil. And they have lived such lives for 2 years now, which is the average life expectancy for lab mice. Detailed biochemical studies show that the designer mice simply burn more fat than their normal counterparts.

If Dr. Wakil's results in mice hold true for humans, then a drug that blocks the function of ACC2 might allow people to lose weight while maintaining a normal diet. The study, which grew out of a desire to determine the different roles of ACC2 and its relative, ACC1, also sheds light on the normal pathways used to metabolize fat.

Image of Mice

When allowed to eat as much as they'd like, normal mice (left) tend to become overweight. Under the same conditions, mice lacking the ACC2 enzyme (right) actually eat more food but remain thinner.


1 Statistics Related to Overweight and Obesity. National Institute of Diabetes and Digestive and Kidney Diseases, NIH Publication No. 96-4158, July 1996.

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