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New Drug: Eat As Much As You Like and Stay Slim

By reducing the amount of insulin, subjects stayed lean.

Live lean and prosper. New research raises the possibility that drugs might be developed to make human fat cells less sensitive to insulin, allowing people to eat as much as they like and still stay slim.

The research, done on genetically altered mice at Harvard Medical School in Boston, blocked sensitivity to fat cells, which allowed the mice to eat what they wanted and yet remain lean. They also lived longer than mice that weren't genetically modified.

An estimated 60 million American adults are overweight, and millions more are at risk to join them.

"Since insulin is needed to help fat cells store fat, these animals had less fat and were protected against the obesity that occurs with aging or overeating," said Dr. C. Ronald Kahn, a professor of medicine and researcher at Harvard's Joslin Diabetes Center and leader of the study team.

"They were also protected against the metabolic abnormalities associated with obesity, including Type 2 (insulin resistant) diabetes," Kahn added. The National Institute of Diabetes and Digestive and Kidney Diseases sponsored the research.

The study, published last week in the journal Science, worked with a new strain of mice, called FIRKO mice (fat-specific insulin receptor knockout), ate normal diets, but had reduced fat mass - 50-to-70 percent less than controls.

And they were protected against obesity and its related metabolic disorders, including Type 2 diabetes, which leaves too much sugar unprocessed in the blood and is usually associated with obesity.

Even when the mice were stimulated to overeat, they didn't gain weight. They had a life span increase of 18 percent, or 134 days, over the control group. The researchers found that at 30 months of age, when 45 to 54 percent of the control mice had died, 80 percent of the FIRKO mice were still alive.

Scientists have observed in a number of experiments that eating less seems to delay aging, perhaps by decreasing metabolism and the related production of harmful "free-radical" molecules that contribute to aging.

But it has not been clear if diet restriction increased longevity directly or whether the longevity was because of being lean. Other factors, including genetics and environmental factors also contribute to life span, but in the FIRKO mice, the researchers feel the altered insulin signal played a key role.

"If we were able to find a drug to reduce or block insulin action in fat cells in humans, we might be able to prevent obesity as well as Type 2 diabetes," Kahn said. "And who knows, they might also live longer."

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