Mitochondrial Dysfunction Model in the Pathogenesis of Inflammatory Response Development in Obesity

Abstract

Obesity is one of the growing problems of modern society. Although currently used methods of treating obesity, including diet, exercise, and drug therapy, have shown their applicability to more effectively combat obesity, an understanding of the pathogenesis of this disease is required. One of the insufficiently studied factors in the pathogenesis of obesity is the development of mitochondrial dysfunction understanding the role of which in the development of obesity will make it possible to find new ways to combat this disease. The review was created by analyzing evidence from the most promising studies on the pathogenesis of obesity. The main aim of this review was to develop a model of the pathogenesis of obesity, the central link in which is the development of mitochondrial dysfunction. An additional aim was to propose, based on the developed model, a number of potential therapeutic strategies for the treatment of obesity. Increased nutrient intake leads to the disruption of the electron transport chain work, which causes an increase in the production of reactive oxygen species, which causes: (1) Damage to mitochondria and as a result, mitochondrial dysfunction, impaired energy metabolism, and increasing oxidative stress, (2) As well as damage to other cellular structures and as a result, the accumulation of toxic oxidation products and immunogenic molecules. Together, this leads to chronic inflammation and the development of insulin resistance, which is the high-risk factor for diabetes. Compounds aimed at normalizing the function of mitochondria, such as L-carnitine and ubiquinone, can be proposed as additional therapies. Aerobic exercise also contributes to the normalization of mitochondrial function.