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Modulation of the autophagic process by high fat diet

Grant number: 13/13480-0
Support type:Scholarships in Brazil - Post-Doctorate
Effective date (Start): August 01, 2014
Effective date (End): July 31, 2017
Field of knowledge:Health Sciences - Nutrition - Nutrition Biochemistry
Cooperation agreement: Coordination of Improvement of Higher Education Personnel (CAPES)
Principal Investigator:Mário Roberto Maróstica Junior
Grantee:Carla Evelyn Coimbra Nuñez
Home Institution: Faculdade de Engenharia de Alimentos (FEA). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
Associated scholarship(s):15/23491-5 - Expression of autophagy genes in Ffar4 knockout mice, BE.EP.PD


AbstractThe expansion of obesity and its associated comorbidities, as insulin resistance, has reached alarming levels and constitutes an emergent public health problem. The ingestion of fat rich diet leads to physiological and immune changes that determines adipose tissue hypertrophy and inflammation establishment. The qualitative change in which saturated fat acids are elevated and capable of activating the TLR4 receptors has been identified as the main factor that contributes to pro-inflammatory alterations associated with high fat diet. On the other hand, the unsaturated fatty acids É-3 are related to reduced inflammation. In this context, the autophagy emerges as an "immunologic paradigm" which is activated by a large array of immune sensors and contributes to the restriction as well as the amplification of the inflammatory signaling. Autophagy is positively stimulated by the TLR4 receptor. This receptor is activated by lipopolysaccharides from gram positive bacteria (LPS) as well as by free fatty acids and are directly linked to the inflammatory signal propagation in metabolic diseases. On the other side, the É-3 fatty acids are capable to block the TLR4 signaling. Thus, knowing how autophagy is modulated in response to different dietary fatty acid compositions could contribute not only to the understanding of the autophagic mechanism, but also to understand the relationship between fatty acids and metaiinflammation physiopatogenia. (AU)