Mechanism of the effect of intermittent fasting on cell aging has been discovered

The central role in this process is played by the NHR-49 protein, which acts as a sensor for lipid levels in cells. During fasting, this protein is activated, initiating the breakdown of fats for energy production due to a lack of glucose. However, in order to achieve the longevity effect, it is crucial to inactivate NHR-49 at the time of food intake. This process is carried out by the enzyme KIN-19 (protein kinase CK1 alpha 1) through phosphorylation. If this mechanism is disrupted and NHR-49 remains active during feeding, the positive effect of fasting on life expectancy is completely negated.

Experimental data showed that even when NHR-49 was genetically removed, fasting increased the life expectancy of worms by 41%, and their behavior remained more active and “young.” This confirmed the hypothesis that it is the body’s ability to effectively stop lipid breakdown and transition to reserve restoration that serves as a biological trigger for longevity. Thus, it is not the depletion of reserves that is crucial, but the precision of the molecular switch at the moment of transition from hunger to satiety.

This discovery allows us to view aging not as an inevitable process, but as a target for preventive medicine. Understanding the molecular link between lipid metabolism and cell degradation opens up the possibility of creating drugs that can mimic the effects of fasting without the need for strict diets. This could lead to the development of therapeutic strategies aimed at improving the quality of life and reducing the risk of age-related diseases by artificially manipulating metabolic phases.