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We know that lifespan can be extended in some animals by restricting calories such as sugar intake shortly after birth. Université de Montréal scientists now say that it's not sugar itself that is important in this process but the ability of cells to sense its presence.Aging is a complex phenomenon and the mechanisms underlying aging are yet to be explained. What researchers do know is that there is a clear relationship between aging and calorie intake. For example, mice fed with half the calories they usually eat can live 40 percent longer. How does this work?As part of the study, Université de Montréal Biochemistry Professor Luis Rokeach and his student Antoine Roux discovered to their surprise that if they removed the gene for a glucose sensor from yeast cells, they lived just as long as those living on a glucose-restricted diet. In short, the fate of these cells doesn't depend on what they eat but what they think they're eating.There are two obvious aspects of calorie intake: tasting and digestion. By the time nutrients get to our cells there is an analogous process: sensors on the surface of the cell detect the presence of, for example, the sugar glucose and molecules inside the cell break down the glucose, converting it to energy. Of these processes, it is widely thought that the by-products of broken down sugars are the culprits in aging. The study by Rokeach and Roux suggests otherwise.Longer chronological life span correlates with higher mitochondrial respiration and increased oxygen stress resistance, except with Gpastrain where loss of survival correlates only with weaker oxidative stress resistance. (A) CLS of doi:10.1371/journal.pgen.1000408