WASHINGTON, Jan 24: Dieters got a bit of hope on Friday from a study that shows a change in a single gene in mice allows them to eat as much as they want while staying thin — and living longer in the bargain.

Many studies have shown that animals live longer when they eat, on average, about 30 percent less than normal. The findings have led scientists to speculate that people, too, can extend their lives by dieting.

But no one quite understands why semi-starvation can help an animal live longer. Studies suggest it seems to have something to do with insulin and metabolism. One theory has been that if an animal eats less, the body produces fewer cell-damaging “free radicals” as a byproduct of metabolizing food.

Dr. C. Ronald Kahn of the Joslin Diabetes Center at Harvard Medical School and colleagues genetically engineered a mouse that lacked a gene called fat-specific insulin receptor. This change limited the action of insulin on fat cells.

The mice, which they nicknamed FIRKO mice (for fat-specific insulin receptor knock-outs), fed freely without gaining much fat and also lived longer than normal mice.

They had 50 to 70 percent less fat, no matter what they ate, and also were less likely to develop diabetes than normal mice. They lived on average 134 days, or 18 percent longer than normal mice. By the age of 30 months half the normal mice had died but 80 percent of the FIRKO mice were still alive.

Writing in the journal Science, Kahn and colleagues said their research suggests it might be something unique to fat that affects life span in animals.

“The concept that most people thought about is that free radical damage might be coming from dietary toxins,” Kahn said in a telephone interview.

“I don’t know whether the free radical theory is out, but we need to think about, could fat itself be producing something that might be leading to free radical damage.”

KEY TO LIFE: Insulin is of course key to life — people with type-1 diabetes, who do not produce insulin, will die without regular injections of the hormone. Kahn said his mice survived well because their bodies block the action of insulin in just one place — the fat cells.