They focused their studies on worms, in which the insulin pathway controls both reproduction and aging. Mutations in the DAF-2 insulin-like receptor prolong the lifespan of a worm, but reduce its fertility. The new data indicate that with good timing, this need not be the case. The group used RNA interference to reduce daf-2 levels, thereby disrupting insulin signaling, at discrete developmental stages. Disruption of DAF-2 during adulthood extended lifespan without affecting reproduction. The time of onset and duration of reproduction, on the other hand, was set by DAF-2 signaling during development, so later disruption had no effect.
There are some arguments for conservation of the system in other species. Mice with low levels of the insulin-related IGF-1 live longer and, says Dillin, “the insulin pathway in worms is almost identical to [the pathway in] humans.” But the elusive fountain of youth is not exactly within reach. The relationship between insulin signaling and aging in humans has not been established, and interfering with all aspects of insulin signaling in humans would induce diabetes. Thus, researchers would first have to find an aging-specific component in humans. The consequences of shutting down such a component also remain unknown. Fortunately, daf-2 worms do not seem to suffer from a general metabolic slowdown; otherwise, an antiaging drug might turn out to be a big snooze. ▪