| Grant number: | 14/01246-6 |
| Support Opportunities: | Scholarships in Brazil - Doctorate |
| Start date: | June 01, 2015 |
| End date: | December 31, 2018 |
| Field of knowledge: | Health Sciences - Physical Education |
| Agreement: | Coordination of Improvement of Higher Education Personnel (CAPES) |
| Principal Investigator: | Fábio Santos de Lira |
| Grantee: | Loreana Sanches Silveira |
| Host Institution: | Faculdade de Ciências e Tecnologia (FCT). Universidade Estadual Paulista (UNESP). Campus de Presidente Prudente. Presidente Prudente , SP, Brazil |
| Associated scholarship(s): | 17/08530-0 - The influence of PPARg on incorporation of fatty acids into placental lipid pools and their transfer to the fetus, BE.EP.DR |
Abstract Moderate aerobic exercise is increasingly established as an effective non-pharmacological therapy for the prevention and treatment of aseptic chronic inflammatory diseases considered as the largest cause of death worldwide. Among these diseases, can be mentioned obesity, diabetes type 2, cardiovascular diseases in general, cancer, neurodegenerative diseases, among others. The therapeutic role of exercise training is through increased anti-inflammatory response induced by moderate exercise. Although this effect is well documented in the literature, little is known about the molecular pathways that may be involved in this process as well as whether the high intensity training is able to modulate the inflammatory response in a similar way of moderate exercise. Macrophages when chronically activated favor the onset and progression of many inflammatory diseases. There are many transcription factors that regulate the response of this cell type, including peroxisome proliferator-activated receptor gamma (PPAR-gamma), which is capable of regulating the immuno metabolic response, leading to an increase in macrophages that are characterized by M2, or is phenotypically presenting an exponential increase in the capacity to secrete anti-inflammatory cytokines and prostaglandins. This change in phenotype occurs as a result of exercise training, we aim to understand whether the PPAR-gamma is important in this process, and finally to assess whether their deletion in myeloid cells may lead to decreased anti-inflammatory response caused by exercise when a low inflammatory state level is induced, in case it occurs, by the induction of obesity in mice. To test our hypothesis, two strains of animals will be used: CreLox for PPAR-gamma (Cre + / + PPAR-gamma - / -) that lead to deletion of PPAR, specifically in myeloid cells, and animal control littermates (Cre - / - PPAR-gamma + / +). For each group of animals will be formed six subgroups with 10 animals per group: 1) balanced diet and sedentary (BS); 2) balanced diet and moderate-intensity training (BTM); 3) balanced diet and high intensity training (BTA); 4) high-fat diet and sedentary (HS); 5) high-fat diet and moderate-intensity training (HTM); 6) high-fat diet and high intensity training (HTA). Will be assessed the metabolic profile and systemic inflammation, as well as primary cultures of peritoneal macrophages, cytokine production and gene expression, protein expression and activation of PPAR-gamma. Experiments with cultured peritoneal macrophages (in vitro) and animal model will provide better understanding of the role of PPAR-gammain immune metabolic regulation. (AU) | |
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