Their work with fruit flies found that calorie restriction and particular mutations in a gene called rpd3 appear to work together to lengthen the insects' lives. Both dieting flies and those with mutant rpd3 showed increased activity in a gene called Sir2, already thought to be a major player in the link between low-cal living and longer life.

Scientists hope that by unraveling the cellular mechanisms by which dieting stretches the life span, they can eventually find a way to "mimic" some of the health benefits of calorie cutting--without the obstacle of having to actually eat less.

But, "the emphasis is on the word 'eventually,"' said study author Stewart Frankel, of Yale University School of Medicine in New Haven, Connecticut.

He told Reuters Health that he and his colleagues at the University of Connecticut believe that rpd3 and Sir2 are the "master switches" of the mechanism by which calorie restriction affects longevity, but there's still a lot to learn about the molecules that carry out the genes' orders.

"We have the coaches, but we need to know who the players are," Frankel explained.

He and his colleagues report their findings in the November 29th issue of Science.

A number of studies have shown that cutting calories extends the life span of yeast, worms, insects and mammals. More importantly, Frankel pointed out, research in monkeys and rodents suggests that it's not only a longer life, but also a healthier one.

As for how calorie restriction might accomplish this, research in yeast and worms has indicated that revved up Sir2 activity is an important factor. In addition, a dip in rpd3 activity has been implicated in bestowing long life to yeast, a single-cell organism.

The new study extends that finding to a more-complex life form, and it also suggests that the drop in rpd3 activity may be particularly crucial, according to Frankel. The findings suggest that low-cal diets lead to decreased rpd3 activity, which is then followed by a boost in Sir2 activity.

Frankel explained that it would easier to design a drug that could lower rpd3 activity, as opposed to one that would jumpstart Sir2.

But a drug that would specifically mimic the life-prolonging effects of calorie cutting would be hard to study in humans, according to Frankel. It would be far easier, he said, to test for a drug that mimics the benefits of calorie cutting upon the diseases of old age.

SOURCE: Science 2002;298:1745.

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