Broken mitochondria are guilty of obesity
Scientists from Immanuel Kant Baltic Federal University on the base of literary sources have described in detail the connection between intracellular processes in mitochondria and metabolic disorders in human's organism that lead to obesity and cardiovascular diseases. Results of the research, supported by the grant of Russian Scientific Fund are published in International Journal of Molecular Sciences.
Obesity is a factor of development of metabolic syndrome, that is characterized by such complications as elevated blood pressure and high cholesterol level in blood. Besides this, metabolism disorders are premonitory signs of principal diseases, that are associated with high mortality in developed countries: cardiovascular diseases and diabetes. According to WHO prevalence of metabolic syndrome among adults consists more 25% and increases each year. It increases five-fold the risk of development of type 2 diabetes, thrice—infarct and twice—probability of death.
Mitochondria with destroyed functions, that means "energetic stations" of a cell that work incorrectly play the vital role in development and progression of diseases connected with metabolic syndrome. In particular, to pathologies lead disorders connected with mitochondrial genome—mtDNA. Inspite of obtained results and new information in the sphere of studying of components of metabolic syndrome and mitochondrial disorders connected with it, many functional questions are still unsolved and demand more detailed analysis. According to scientists, molecular-genetic researches, that are focused on biology of mtDNA and processes of its reconstruction, enable to find effective personalized solution for prevention and struggle with heterogenic phenotype of metabolic syndrome.
What mitochondria do with all this and why are they to blame? Each cell contains many mitochondria—energetic stations, where the process of cell breathing and production of ATP takes place. ATP is an important molecule without which every living organism can't normally function. There is one more interesting detail: its own DNA (mtDNA), that differs from common human DNA from cell nucleus, is hidden in mitochondria. Such difference is connected with origin of mitochondria from bacteria. Thus, the condition of an organism influences integrity of mitochondria and their genetic information. For example, when there is inflammation in fatty tissue, mtDNA begins to destroy, because special cells are trying to extinguish an inflammatory process, and so cause resistibility to insulin, and, as a consequence, distortion of integrity of mitochondria.
It should be noted that people with heart diseases more often have deficit of mtDNA, without which mitochondria can't function in full force, and consequently will give less energy for organ's work. Further researches, that will be conducted in larger populations in different countries, can help to define molecular-genetic connections between changes in mtDNA and distortions of metabolic syndrome more precisely and fill the gaps in information about pathogenesis of this disease. At the same time study of reduction potential of cells, especially their mitochondria, can help to elaborate a system of diagnostics of metabolic distortions and find out target molecules for pathogenetically substantiated treatment.
"Mitochondria are unique intracellular organelles, that contain their own—mitochondrial DNA (mtDNA), that differs from nuclear genome. When a person suffers from obesity, there occurs reduction of number of copies of mtDNA in cells, its fragmentation, mutations and output of mtDNA from mitochondria and cells. All these lead to reduction of breathing system of mitochondria, development of inflammatory reaction, aging of cells and tissues, and also to development of such conditions as insulin resistance, type II diabetes mellitus, cardiovascular diseases, metabolic syndrome. However, in cell exist special enzymes, that are able to reconstruct functions of mitochondria and protect their genome from damages. Such enzymes can become a base for obtaining new drugs against diseases connected with metabolic syndrome", -summed up the author of the review, Natalia Todosenko, research associate of Basic Laboratory of Immunology and Cell Biotechnology of Immanuel Kant Baltic Federal University.
Provided by Immanuel Kant Baltic Federal University