| Grant number: | 13/23072-7 |
| Support Opportunities: | Scholarships in Brazil - Master |
| Start date: | May 01, 2014 |
| End date: | April 30, 2016 |
| Field of knowledge: | Biological Sciences - Physiology - Physiology of Organs and Systems |
| Principal Investigator: | Adriana Souza Torsoni |
| Grantee: | Fernanda Oliveira Borges |
| Host Institution: | Faculdade de Ciências Aplicadas (FCA). Universidade Estadual de Campinas (UNICAMP). Limeira , SP, Brazil |
Abstract The obesity has acquired epidemic characteristics and the same numbers that indicate the increase in obesity also showed a significant increase in individuals with diabetes mellitus type 2. It is now known that both diseases exhibit a metabolic response characteristic, which leads to changes in intracellular signaling pathways and glucose homeostasis. High fat diet (HFD) consumption is responsible for the increased fat mass leading to an increased production of pro-inflammatory cytokines. Several studies indicate the involvement of macrophages in this process. The non-canonical NF-ºB pathway contributes to the pro-inflammatory signaling activation, and may represent a key metabolic pathway in response to obesity, especially in insulin resistance. Our hypothesis is that the nutritional overload trigger macrophage polarization in metabolic tissues and activation of NIK by blocking of TRAF-3 on immune cells (such as Kupffer cells), resulting in an increase in pro-inflammatory cytokines expression. To test this hypothesis, we will employ co-culture of monocytes cells and hepatocytes treated with NIK siRNA, and challenged with palmitic acid or LPS, in order to confirm the importance of communication between hepatocytes and liver macrophages in the development of insulin resistance. (AU) | |
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