To investigate if CDAA was worsening also NTNCB hydrochloride hepatic insulin resistance, we have measured the expression of liver enzymes associated with glucose production, gluconeogenesis and de-novo lipogenesis as SREBP-1c and ChREBP. The results show that G6Pase and PEPCK mRNA expression was decreased, indicating a parallel decrease in glucose production. This is in agreement with the observed reduction in FPG and possibly due to the increase in fasting plasma insulin that is known to suppress both glucose production and gluconeogenesis. ChREBP and SREBP-1c expressions were also reduced indicating that de-novo lipogenesis was not directly implicated in the development of liver steatosis. On the other hand, the reduction in ACOX-1 and CPT1A indicates that CDAA diet reduced hepatic fatty acid STEARDA oxidation and this could be one of the mechanisms for hepatic triglyceride deposition and for the higher lipid deposition in CDAA+CCl4 treated animals, presumably mediated by TGFb signaling in hepatocytes. Thus, we can conclude that CDAA induces steatosis mainly by reducing FFA oxidation, while neither de novo lipogenesis nor glucose production seem to play an important role. Despite the intrinsic differences among etiological factors for HCC, a common denominator at the origin of this neoplasia is the perpetuation of a wound-healing response triggered by parenchymal cell death, the ensuing inflammatory reaction and the concomitant fibrosis progression. Indeed, HCC almost always develops on a background of chronic liver injury including chronic hepatitis and cirrhosis, conditions referred as preneoplastic stages. Accumulating evidences indicate that the inflammatory reaction characteristic of chronic liver injury actively participates in the development of hepatic fibrosis, as well as in the activation of the potent regenerative response of liver parenchyma, ultimately leading to HCC development. For instance, the production of cytokines such as TNFa and IL-6 is essential to trigger hepatocyte proliferation, liver regeneration and animal survival after partial hepatectomy. On this regard, in our model we observed an higher number of infiltrating macrophages and this was accompanied by a complete repertoire of the inflammatory response such as apoptotic cells, TNFa, MCP-1 and components of the Inflammasome pathway gene expression.