| Grant number: | 16/01409-8 |
| Support Opportunities: | Regular Research Grants |
| Start date: | June 01, 2016 |
| End date: | May 31, 2018 |
| Field of knowledge: | Health Sciences - Nutrition - Nutrition Biochemistry |
| Principal Investigator: | José Cesar Rosa Neto |
| Grantee: | José Cesar Rosa Neto |
| Host Institution: | Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil |
| City of the host institution: | São Paulo |
Abstract
The obesity is na epidemic condition in developed and development countries. The high consumption of fat acids in ocidental diet, and the sedentarism induced the body weight gain, and the accumulation of fat acids in depots of adipose tissue, and other organs, such as liver. This condition caused the low grade inflammation, condition that it is presented in the genesis of co-morbidates associated with obesity. The excess of fat acids are depot in hepatic parenchyma, with increased in severity of liver damage. Recently, the palmitoleic acid demonstrated the positive effect in restored of glucose and insulin intolerance, and attenuation in liver inflammation in obese mice, and humans. These effects could be modulated by PPAR family, whereas the PPAR alfa increased the hepatic fat acids oxidation, and the PPAR gamma promoted the fat acids accumulation, but the two isoforms showed anti-inflammatory properties. The aim of our study is elucidate the molecular mechanisms of anti-inflammatory supplementation of palmitoleic acid in liver of obese mice. We utilized the C57BL/6J mice that will be divided into 4 groups: control group; control group + palmitoleic (oral gavage); high fat group; and high fat + palmitoleic. We will evaluate the insulin sensitivity, liver histology, and inflammation in liver, the types of macrophages infiltrated and the inflammation in hepatocytes and macrophages. In culture cells, of primary intraperitoneal macrophages and hepatocytes we will utilize inhibitor of PPAR alpha and gamma, with addiction of palmitoleic acid conjugated with BSA, in stimulated condition by LPS. We will analyze the cytokines production (in vivo and in vitro models), the molecular pathway (NFºB and JNK), the subsets of macrophage infiltration in liver by flow cytometry; and the expression of enzymes that regulated the lipids mediators (COX-1;COX-2:LOX5 and LOX12/15). (AU)
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