Interdisciplinary collaboration between two researchers Institutes of the Institute of Technology and Research (FORTH), of the Institute of Molecular Biology and Biotechnology (IMBB), in Heraklion and of the Institute of Chemical Engineering (IEXMI), in Patras, sheds light on a new mechanism for regulating aging, through reprogramming of cellular metabolism. The new findings published today in one of the most prestigious international scientific journals, Nature Communications, are expected to help develop applications aimed at treating metabolic diseases and pathologies that accompany aging.
According to the announcement of FORTH, the metabolism is the complex network of biochemical reactions that convert the energy received by an organism through food into chemical energy that can be used by cells. It is a fundamental biological process, absolutely necessary for the development and maintenance of life. The cellular organelle that is primarily responsible for the production of chemical energy in all eukaryotic cells is the mitochondria. In addition, it is reported that the final stages of glucose breakdown, one of the basic carbohydrates that metabolize cells, take place in the mitochondria. It is important that the basic metabolic processes are closely linked and largely determine the rate of aging.
Using the nematode Caenorhabditis elegans as an experimental system, the IMBB Researchers, Dr. Irini Lionaki, Dr. Elias Gikas, Dr. Ioanna Daskalaki and Dr. Nektarios Tavernarakis (Professor of the Medical School of the University of Crete, in collaboration with Konstantina Ioannidi and Dr. Maria I. Klapa (IEXMI), revealed that reducing the number of mitochondria in specific tissues significantly increases life expectancy.
“This reduction in mitochondrial mass, which can be achieved with appropriate genetic or pharmacological interventions, is inextricably linked to a reduction in the production of oxygen free radicals, the activation of stress response mechanisms and an increase in glucose uptake from the environment. Analysis of the metabolic profile in experimental animals with increased lifespan revealed specific metabolic changes that redefine the way they use glucose, inducing the production of another metabolite, serine. Serine is an amino acid that can be produced from glucose through a series of biochemical reactions. Inhibition by appropriate suppressors of this enzyme sequence of serine production negates the benefits of reduced mitochondrial number in survival expectancy, restoring a cause-and-effect relationship between cell mitochondrial contents, and announcing serocyte production.
It is known that prolonged exposure to high glucose levels is associated with the development of serious metabolic diseases, such as obesity and diabetes. In their new study, FORTH researchers show that increased glucose uptake significantly reduces survival expectancy, increasing oxidative stress. In contrast, interventions to reduce mitochondrial mass in specific tissues protect against glycotoxicity and significantly improve survival under conditions of exposure to elevated glucose levels.
“The results of research published today, highlight the complexity of the aging phenomenon, leading to a revision of previously simplified perceptions of how aging is affected by genes and the environment. The findings of the study are crucial for understanding aging in humans, and are expected to be used to treat comorbidities, which are characterized by metabolic disorders, with targeted therapeutic interventions, aimed at improving the quality of life in old age. the announcement concludes.
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