1259 CELL CYCLE ARREST AND ACCELERATED TELOMERE SHORTENING IN NON-ALCOHOLIC FATTY LIVER DISEASE (NAFLD)

were fed a standard diet (SD). Blood and tissue samples were used for histological, biochemical and molecular analyses. HepG2 cells were used as a model to study molecular pathways that control LITAF expression/activity. Results: We found that either LITAF mRNA or protein were enhanced in the liver of HFD-HF rats, concomitantly with an increased expression of TNF-a mRNA, and augmented serum levels of LPS and TNF-a. Noteworthy, the immunohistochemical analysis showed that LITAF expression increased in liver from HFD-HF rats, and in liver tissues from 12 children with respect to their respective control samples (SD rats and healthy individuals). Furthermore, we found an increased phosphorylation and nuclear translocation of LITAF in HFD-HF rats. In HepG2 cells, we found that the LPS-induced expression of LITAF was susceptible to the silencing of p53 (by siRNA), while LPSinduced activity of LITAF was affected by the inhibition of p38MAPK. This last data was also supported by the increased p38MAPK phosphorylation in HFD-HF rats. Conclusions: In conclusion, we demonstrated that liver damage in enriched fructose high-fat diet is associated with increased serum levels of endotoxin and TNF-a, and we suggested, for the first time, a possible role of LITAF as promoter of inflammatory liver response to bacterial endotoxin in NAFLD.