Role of physical training on UPRmt in musculature skeleton of obese mice

• Grant number: 22/00388-8
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: April 01, 2022
• End date: December 31, 2022
• Field of knowledge: Health Sciences - Medicine
• Principal Investigator: Eduardo Rochete Ropelle
• Grantee: Sidney de Figueiredo Peres
• Host Institution: Faculdade de Ciências Aplicadas (FCA). Universidade Estadual de Campinas (UNICAMP). Limeira , SP, Brazil
• Associated research grant: 19/21709-4 - Implications of mitonuclear imbalance and UPRmt in hypothalamic neurons in the genesis of Obesity, AP.TEM

Abstract

Mitochondria are the main site of intracellular energy production, according to the endosymbiotic theory, it originated from a bacterium that at some point was engulfed by the process of endocytosis by eukaryotic cells. As the relationship symbiotic relationship was of mutual benefit, this association prevailed, the main advantage of to keep the mitochondria incorporated, it was because of its function of being able to produce energy from ATP. This important enzymatic machinery that produces ATP by through oxidative phosphorylation (OxPhos), has a refined responsible for importing, transporting, folding and assembling the protein complexes necessary for its functioning (through the chaperones), and when necessary, capable of degrading proteins that are not working properly (through proteases). This control system can be stress-induced causing the UPRmt(mitochondrial unfolded protein response), which is associated with the best functioning of the mitochondria and with the increase in their number, reflecting on the function oxidation of skeletal muscle, for example, and directly interconnected with the ability of mitochondria to survive under stress, restoring the proteostasis. It is known that obesity is closely linked with dysfunction mitochondria (malfunction of the OxPhos complex) and in the development of other metabolic diseases. Studies indicate that changes in mitochondrial function is a factor key in the regulation of metabolic diseases such as obesity and diabetes. Like the aerobic physical exercise is also a stressor agent and contributes to the improvement of oxidative capacity of the organism, we put forward the hypothesis that physical exercise aerobic activity activates the UPRmt contributing to an improvement in the function of mitochondria, so that there is better oxidative capacity in the skeletal muscle of mice obese, considering that the practice of physical exercise is a non-pharmacological to prevent and/or treat several other existing metabolic disorders and diseases, it may contribute to the alteration of mitochondrial dysfunction in the context of obesity.(AU)