In order not to get old, do not think about sweet things :-)
Glucose accelerates aging even before it is involved in metabolismCanadian scientists have discovered that the signaling pathway that accelerates aging in dividing yeast is not associated with glucose processing by the cell, but with a receptor on the membrane that senses the presence of this substrate in the external environment.
That is, the rate of aging of a cell depends not on what it eats, but on what it "thinks" it eats.
We have repeatedly written (see, for example, this article) that food restrictions prolong the life of various organisms. The main source of energy and carbon for heterotrophic organisms is glucose (it should be said that this is practically the only source of energy for the neurons of the central nervous system), but its excess is associated with the aging process, and the lack slows it down. Scientists from the University of Montreal (Université de Montréal) have discovered that life expectancy is influenced not by the metabolic processes occurring with glucose in the cell, but by the cell's feeling of its amount outside.
Louis Rokeach, Antoine Roux, Pascal Chartrand and Gerardo Ferbeyre study aging on dividing yeast Schizosaccharomyces pombe. Their aging is quite similar to the aging of human cells, especially at the molecular level. These yeasts also have an increased lifespan and resistance to oxidative stress with a decrease in glucose consumption. The researchers found that if you remove the G-protein-bound Git3 membrane glucose receptor gene, the cells live as long as when they limit their glucose intake. At the same time, cells that are unable to consume glucose as an energy source (hexokinase mutation, Hxk1/2) remain sensitive to its aging-accelerating effect. Constitutive activation of the G-protein, through which the signaling pathway activated by Git3 goes, leads to a weakening of the effect of an increase in life expectancy caused by glucose restriction. The mechanism of accelerating aging through the glucose receptor Git3 consists in increasing the amount of reactive oxygen species and reducing resistance to oxidative stress and respiration rate (oxidation of sugars with oxygen).
Two ways glucose affects aging through the production of free radicals in mitochondria
The signaling pathway from the G protein is transmitted via adenylate cyclase to protein kinase A (PKA) activated by cyclic adenosine monophosphate (cAMP). Its activation causes the accumulation of reactive oxygen species (ROS) in the mitochondria, which cause aging. In more primitive budding yeast and the roundworm Caenorhabditis elegans, there is also a direct pathway for the effect of phosphorylated glucose hexokinase on respiration efficiency and the production of free radicals in mitochondria (the so-called glucose repression pathway), but in dividing yeast, judging by the results of the study, this signaling pathway does not affect the acceleration of aging by glucose.
This seemingly harmful signaling pathway may have an evolutionary significance. With a large amount of food resources, a population can afford to accelerate evolutionary processes by reducing the lifespan of an individual organism, and with their scarcity, when there is not enough energy for reproduction, the preservation of the genotype depends on the survival of this organism, and its lifespan increases.
The results of the study will help to develop new therapeutic strategies for diseases associated with aging. These may be pharmacological blockers of the glucose receptor or gene therapy aimed at weakening the expression of this receptor.
Sources:
EurekAlert: Not so sweet: Over-consumption of sugar linked to aging – 5-Mar-2009
Roux AE et al. 2009 Pro-Aging Effects of Glucose Signaling through a G Protein-Coupled Glucose Receptor in Fission Yeast. PLoS Genet 5(3): e1000408 (free access article)
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18.03.2009