Disruption of tumor necrosis factor alfa receptor 1 (TNFR1) signaling pathway increases interleukin-1 beta levels, exacerbates hepatic inflammatory response and apoptosis during a high fat diet (HFD)

ARBOATTI A; ROGGERO E; CARNOVALE C E; LAMBERTUCCI F; VILLAR S; ALVAREZ ML; FRANCÉS D E; SEDLMEIER MG; CEBALLOS M P; QUIROGA A D; RONCO M T

Mar del Plata

Congreso; LXI Reunión Científica Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2016

SAIC

One hallmark of obesity is chronic low grade inflammation and increased pro-inflammatory circulating cytokines, which play an important role in the development of insulin resistance (IR). Obesity associated hepatic inflammation is due to increased Kupffer cell activation and recruited hepatic macrophages. Sustained inflammation may increase the susceptibility of hepatocytes to apoptotic cell death and therefore exacerbate liver damage. In this work, weaim to study hepatic TNFR1 receptor association with inflammation and apoptosis in a model of IR and altered energy homeostasis induced by HFD. C57BL/6 wild type (WT) and TNFR1 knock-out (KO) mice (n=6) were fed with regular chow diet (CHOW-WT, CHOW-KO) or a 40% high-fat diet for 16 weeks (HFD-WT, HFDKO). Here, we report that after 16 weeks of HFD, the plasmatic levels of interleukin(IL)-1β were increased by HFD especially in KO mice (HFD-KO: 189 pg/ml; HFD-WT: 1078 pg/ml; p