Forget the drastic reduction in carbs and calories called for by diet dictators. The day when people can eat their favorite foods, stay thin and live to be 120 without getting age-induced diabetes or cancer may be nearer than we think. Researchers at MIT believe they've found the key to a long, lean, healthy life in a single protein that controls whether a mammal stores fat or sheds it. The work could lead to drugs that mimic that protein, allowing human beings to get the longer lifespan and other benefits of extreme caloric reduction without the negative side effects, said MIT Professor of Biology Leonard Guarente.

Guarente and other scientists have known for decades that controlled famine can extend the lifespan of mammals by as much as 50 percent and that those long-lived, lean mammals don't get the diseases of old age.

But just how a vastly reduced caloric intake achieves that feat has been a mystery begging for a solution--until now.

"For the first time, this study gives us a glimpse of how calorie restriction works at the molecular level. And it will ultimately lead to health benefits in people," said Guarente, who has been studying the aging process in yeast, roundworms and mice for more than a decade.

In the June 2 online issue of the journal Nature, scientists in Guarente's lab, including Frdric Picard, a research scientist in the Department of Biology who is lead author of the paper, publish their research results about how the Sirt1 mammalian gene promotes fat mobilization in mice.

A mammal generally burns the protein and carbohydrates in its food immediately; it stores fat in special cells called white adipose tissue (WAT). When it reduces its caloric intake, the WAT stops storing fat and begins releasing it for metabolism.

The paper's authors learned that fat is released from or metabolized by the body, rather than stored, when the Sirt1 protein senses short-term famine and turns off the receptors that
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Contact: Denise Brehm
brehm@mit.edu
617-253-2704
Massachusetts Institute of Technology
2-Jun-2004

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