Nutrient and stress sensors mediate lifespan extensions that occur in response to many different environmental and physiological signals. The best known of these signals is dietary restriction, which extends lifespan in many species, from yeast to primates.
Dietary restriction was initially assumed to extend lifespan simply by reducing the rate at which cellular damage accumulates over time as a result of nutrient metabolism. Recently, however, an elegant experiment with Drosophila showed that dietary restriction produces a rapid decrease in the mortality rate (the daily chance of death), suggesting that dietary restriction counteracts the causes of ageing in an acute manner.
We now know that the longevity response to dietary restriction is actively regulated by nutrient-sensing pathways involving the kinase target of rapamycin (TOR), AMP kinase, sirtuins and insulin/insulin-like growth factor (IGF-1) signalling.
Unexpectedly, which nutrient sensor is most important in extending lifespan in response to dietary restriction depends on the way that dietary restriction is imposed. In C. elegans, for example, one nutrient sensor extends lifespan in response to life-long food limitation, another in response to every-other-day feeding and a third if dietary restriction begins in middle age.
SOURCE: Nature (2010)