- HIGH FAT DIET CONSUMPTION IMPAIR EARLY α7nAChR EXPRESSION IN SPLEEN OF SWISS MICE.

SOUZA, ANELISE CRISTINA PARRAS; LEMES, SIMONE FERREIRA; MILANSKI, MARCIANE; TORSONI, ADRIANA SOUZA; TORSONI, MARCIO ALBERTO

Foz do Iguaçu, Paraná

Congreso; 44th Annual Meeting of the Brazilian Society for Biochemistry and Molecular Biology (SBBq); 2015

INTRODUCTION Antiinflammatory cholinergic pathway can control the inflammatory response. This neural circuit is responsible for converting signals from the brain to peripheral tissues, subunit-dependent manner α7 nicotinic acetylcholine receptor (α7nAChR). High-fat diet-induced obesity and insulin resistance (IR) are associated with inflammation, but the relation between these metabolics disorders and cholinergic antiinflammatory pathway are unclear. OBJECTIVES To determine factors that may cause IR, we have performed a time-course study in mice fed a high fat diet (HFD) MATERIALS AND METHODS Swiss male mice were fed (3 days, 5, and 16 weeks) with standard chow or HFD (60% fat). Body weight, fasting glucose, epididymal fat pad mass, spleen inflammatory cytokines and α7nAChR expression were evaluated DISCUSSION AND RESULTS Body weight, fasting glucose, epididymal fat pad mass, spleen inflammatory cytokines and α7nAChR expression were evaluated. Body mass, fasting glucose and epididymal fat pad mass were significant incresead in HFD compared to SC mice. IL-1β expression was increased after 5 and 16 weeks (2.1-fold and 2.6-fold, respectively) in HFD compared to SC mice. TNF-α gene expression was 1.5-fold higher in HFD than SC mice (5 weeks). α7nAChR gene expression was reduced (3.2-fold) in HFD compared to SC mice (3 days), but for 5 and 16 weeks did not observe difference between groups evaluated. CONCLUSIONS These results show that HFD consumption modulates early (3 days) spleen α7nAChR gene expression compared to proinflammatory cytokines expression (5 and 16 weeks). In this condition the inflammatory response could be elevated and promote damage to tissues. Supported by : CAPES. Keywords: citokynes, α7nAChR, mice