ANN ARBORScientists have known for nearly a century that cold-blooded animals, such as worms, flies and fish all live longer in cold environments, but have not known exactly why.
Researchers at the University of Michigan Life Sciences Institute have identified a genetic program that promotes longevity of roundworms in cold environmentsand this genetic program also exists in warm-blooded animals, including humans.
"This raises the intriguing possibility that exposure to cold airor pharmacological stimulation of the cold-sensitive genetic programmay promote longevity in mammals," said Shawn Xu, LSI faculty member and the Bernard W. Agranoff Collegiate Professor in the Life Sciences at the U-M Medical School.
The research was published online Feb. 14 in the journal Cell.
Scientists had long assumed that animals live longer in cold environments because of a passive thermodynamic process, reasoning that low temperatures reduce the rate of chemical reactions and thereby slow the rate of aging.
"But now, at least in roundworms, the extended lifespan observed at low temperature cannot be simply explained by a reduced rate of chemical reactions," Xu said. "It's, in fact, an active process that is regulated by genes."
Xu found that cold air activates a receptor known as the TRPA1 channel, found in nerve and fat cells in nematodes, and TRPA1 then passes calcium into cells. The resulting chain of signaling ultimately reaches DAF-16/FOXO, a gene associated with longevity. Mutant worms that lacked TRPA1 had shorter life spans at lower temperatures.
Because the mechanisms identified by Xu and his collaborators also exist in a range of other organisms, including humans, the research suggests that a similar effect might be possible. The study also links calcium signaling to longevity for the first time and makes a novel connection between fat tissue and temperature response.
Researchers have known that lowering the core body tempe
|Contact: Laura J. Williams|
University of Michigan