LA JOLLA, CA\u2014Substantial evidence suggests that lifespan is increased if an organism restricts its daily calorie intake, a spartan regime that some say works by just making life seem longer. A team of scientists from the Salk Institute of Biological Studies has discovered a molecular switch flipped by hunger that could not only make longevity more appetizing but identify drug targets for patients with aging-related diseases such as type II diabetes or cancer.\n<\/p>\n
\nIn the February 17, 2011 issue of Naturaleza<\/em> Investigador del Instituto M\u00e9dico Howard Hughes Andrew Dillin<\/a>, Ph.D., an associate professor in the Molecular and Cell Biology Laboratory, and Howard Hughes Medical Institute early career scientist Reuben Shaw<\/a>, Ph.D., an assistant professor in the Molecular and Cell Biology Laboratory and the Dulbecco Laboratory for Cancer Research, report for the first time that deactivation of a protein called CRTC1 in roundworms increases their lifespan, most likely mediating the effects of calorie restriction.\n<\/p>\n \nPreviously, researchers knew hunger promoted longevity by activating an enzyme called AMPK, which senses that food is scarce and pushes cells into a low energy state. “We knew AMPK was a major energy sensor but didn’t know what it was talking to,” says Dillin, one of two senior authors of the study. “Our goal was to understand the genetic circuitry that registered that response.”\n<\/p>\n \nTo define the circuitry, Dillin, who studies aging using the roundworm Ceanorhabditis elegans<\/em> as a model system, joined forces with Shaw, who had a long-term interest in AMPK’s role in mammalian metabolism. “It was clear that one pathway that coordinated metabolism with growth in response to nutrients was AMPK signaling,” says Shaw. “Studies had also suggested that AMPK might regulate lifespan in worms. What was not known was what factors downstream of AMPK mediated those effects.”\n<\/p>\n