The fact that an animal’s lifetime is prolonged by decreasing its sugar ingestion is commonly recognized. In a study published in the journal PLoS Genetics, scientists from the Université de Montréal, reveal that sugar in itself is not the key element but the cells’ capacity to detect its presence is.
The intricate works of the process of aging are still not clearly defined. The link between aging and calorie consumption is certainly obvious to researchers. For instance, why do mice live 40 percent longer when their calorie intake is reduced by half?
Biochemistry Professor Luis Rokeach, Université de Montréal, and his student Antoine Roux, as part of the PLoS Genetics study, were astonished at their findings. They established that after removing the gene of a glucose sensor from yeast cells, the lifespan was the same as for those on a glucose restricted diet. In brief, the outcome of these cells relies on what they think they are eating and not on what they are really eating.
Tasting and digestion are the two main features of calorie consumption. When the nutrients reach our cells, the sensors on the surface identify their presence. For instance, for sugar glucose, the molecules within the cell break down the glucose and transform it into energy. The by-products of broken down sugars are usually blamed for the development of the aging process. However, Rokeach and Roux’s study claims otherwise.
Rokeach and Roux in association with Biochemistry Professors Pascal Chartrand and Gerardo Ferbeyre, Université de Montréal, used a yeast model organism to provide further evidence on aging. Yeast cells are essentially comparable to human cells, their aging process is similar and they can be easily studied.
When glucose was reduced in their diet, the yeast cells’ lifespan increased, according to the findings. The researchers questioned whether the increase in lifespan was a result of the decrease in the cells’ capacity to generate energy or whether it was caused by the drop in signals to the cells by the glucose sensor.
The study established that cells which are not capable of consuming glucose as an energy source are still receptive to the pro-aging effects of glucose. On the other hand, erasing the sensor that evaluates the levels of glucose increased lifespan considerably.
Professor Rokeach says “Thanks to this study, the link between the rise in age-related diseases and the over-consumption of sugar in today’s diet is clearer. Our research opens a door to new therapeutic strategies for fighting age-related diseases.”
Partners in research:
Professor Rokeach’s research is supported by the Canadian Institutes of Health Research and by the National Science and Engineering Research Council. Professor Ferbeyre’s and Professor Chartrand’s research are funded by the Canadian Institutes of Health Research.
“Pro-Aging Effects of Glucose Signaling through a G Protein-Coupled Glucose Receptor in Fission Yeast.”
Roux AE, Leroux A, Alaamery MA, Hoffman CS, Chartrand P, et al. 2009
PLoS Genet 5(3): e1000408. doi:10.1371/journal.pgen.1000408
Click here to see article online
About the Department of Biochemistry, Université de Montréal http://www.bcm.umontreal.ca
Written by Stephanie Brunner (B.A.)