[extropy-chat] A gene that releases stored fat may be the key to a longer life

Giu1i0 Pri5c0 pgptag at gmail.com
Thu Sep 23 13:42:41 UTC 2004


>From Technology Review: On his laptop computer, biology professor
Leonard Guarente plays a video clip of 29-month-old mice hobbling
around a cedar-chip-filled cage. They're scruffy, fat, slow moving,
and over the hill by rodent standards. Then he plays a clip of another
group of 29-month-old mice. They're svelte, frisky, and scrambling
around like adolescents. What's their secret? These mice have eaten
about two-thirds as many calories as their portly peers. Not only does
the meager diet seem to keep them light in the limbs, but they tend to
live 30 percent longer than their well-fed friends and are less likely
to contract age-related diseases, such as diabetes and cancer.

When Guarente first decided to study the causes of aging in the early
1990s, it was a topic tackled by few researchers. No one knew how to
approach it. "The early ideas, which were really quite persistent,
were that if you eat less, everything just slows down," says Guarente.
But he and two postdoctoral students decided to see if they could find
a genetic cause for the phenomenon. In 1996, they found mutant yeast
cells that lived 50 percent longer than normal cells and analyzed
them, gene by gene. "I said, 'We have a year to work on this, because
I'm not sure if there's anything to study,'" Guarente recalls. "We got
really interested, and it took a lot more than a year before I was
sure we had something. We were seduced."
Over the next few years, the researchers tied the unusual longevity in
the mutant yeast to one gene: SIR2. In other experiments, they
discovered that when they inserted extra copies of SIR2 into normal
yeast, it lived longer; when they deleted the gene, the yeast died
prematurely. In 2000, the researchers found that a similar gene in
worms worked the same way. It was exciting, Guarente says, because
yeast and worms are such different creatures that in order to share a
similar gene, they must have had a common ancestor. "That means that
any descendant of that ancestor, including us, has the same
mechanism," he says.
At the very least, mice have it. In their Nature article, Guarente and
his colleagues reported that when food is scarce, a mouse's genetic
equivalent of SIR2, SIRT1, produces a protein that turns off other
genes that help store fat. The fat moves into the bloodstream, travels
to other tissues, and gets burned. This keeps the mice lean and, for
some as yet unknown reason, young looking and healthy into old age.
Frédéric Picard, a research scientist who worked with Guarente on the
paper, remembers the day that he got clear results from the
experiment. "I was very happy, dancing all over. It was great," Picard
says.

http://www.technologyreview.com/articles/04/10/scanlon1004.asp?trk=top



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