The two-faced "aging gene"
The "aging gene" helps to survive
The fat layer will save in frosts, and in a peaceful life it will lead to diabetesNika Kotova, <url>
His presence seems to be necessary for survival in difficult conditions. The reason is that this gene is needed for energy metabolism.
A few years ago, in the laboratory of Pier G. Pelicci from the European Institute of Oncology in Milan, Italy, it was discovered that switching off the p66Shc protein gene in mice leads to a slowdown in aging and an overall increase in viability. Marco Giorgio, who received mutant mice devoid of the p66Shc gene, showed that these mice are slimmer and healthier than their normal relatives and they do not develop age-related diseases.
Further studies have shown that the product of this gene, the protein p66Shc, increases the formation of reactive oxygen species in the body and is involved in pathologies such as diabetes, cardiovascular diseases and metabolic disorders. Mice with the gene turned off have reduced oxidative stress, which has a positive effect on their health and slows down aging.
But this seemingly "harmful" gene is present in all vertebrates. It is unclear why it has been preserved in the process of evolution. And in general, why is it needed? Scientists decided to answer this question.
Further work with mutant mice continued in Russia, at the Clean Forest biostation in the Tver region, with the participation of Swiss and Russian researchers. Mutants deprived of the p66Shc gene were placed together with ordinary mice in a large fenced enclosure in a field. Unlike greenhouse laboratory conditions, mice in this enclosure were subjected to many hardships and difficulties of living in the wild. First of all, the winter cold and birds of prey acted on them as factors of natural selection.
A year later, a genetic analysis of this mouse population showed that the proportion of mutant "ageless" mice decreased sharply, despite the overall increase in the number of animals. There were three times more ordinary mice, and four times fewer mutants than were placed in the aviary at the beginning. This meant that natural selection excluded mutants from the population.
Consequently, the normal allele of the p66Shc gene, although it accelerates the aging of animals, gives significant advantages in a difficult life in natural conditions.
Scientists reasoned that the extinction in the aviary at the biostation could have happened either because of the wrong behavior of mutants, or because of defects in their metabolism. This they began to find out in the laboratory. The behavior of mutants in all tests did not differ from the behavior of normal mice. But in other tests, scientists have found that mutants tolerate cooling and starvation much worse. The combination of these two factors – cold and hunger – in the natural environment simply killed them.
At the metabolic level, it turned out that without the p66Shc gene, mice do not form fat reserves that would protect them in the cold. That's the answer: the "harmful" gene turned out to be necessary for energy conservation. In addition, mutants lacking the p66Shc gene reproduced worse.
Thus, the p66Shc gene is both bad and good, depending on the circumstances. It ensures survival in extreme conditions when fat accumulation is necessary for existence and reproduction. And in ordinary life, when it is not necessary to survive, the accumulation of fat serves a bad service, as it leads to diabetes, cardiovascular diseases, etc.
The researchers published the results of their study in the journal Aging Cell (Giorgio et al., The p66 Shc knockout mice are short lived under natural condition).
The p66Shc gene is not the only "aging gene" known today. Dozens of studies on different animals have shown that switching off certain genes leads to a slowdown in aging and an increase in life expectancy. But this is often accompanied by negative effects (loss of the ability to reproduce, dwarfism, etc.).
"The work of Italian, Swiss and Russian researchers clearly demonstrates that the results obtained in the laboratory may differ from the results obtained in vivo," comments Academician V.P.Skulachev, head of the biomedical project for the development of anti–aging drugs. – We know this well, because we have just completed similar experiments on wild rodents – blind and hamsters, as well as on laboratory mice in conditions close to natural. Based on the results of the experiment, we published an article in the American journal Aging, where we showed that in such "extreme" conditions, the geroprotector we developed (as opposed to the Italian mutation) slows down aging and promotes survival. Now it is becoming more and more obvious that aging is a program controlled by our genes, and not a random accumulation of breakdowns in the body. When we understand how this program works, we will be able to create drugs that can slow down or even stop its work. I am sure that in the next decade there will be a number of effective means in medicine that slow down aging. The first successes on this path are already there now."
Portal "Eternal youth" http://vechnayamolodost.ru13.05.2013