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Introduction: Hepatocellular carcinoma (HCC) accounts for the majority of primary liver cancers. Approximately 5–30% of HCC patients lack a readily identifiable risk factor for their cancer, and most of these cases are attributed to nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Body: Recent lines of evidence have suggested the role of intestinal microbiota, in particular the dysbiosis, in the pathogenesis of chronic liver diseases, such as NAFLD/NASH. Intestinal microbes produce a large array of bioactive molecules from mainly dietary compounds, establishing an intense microbiota-host transgenomic metabolism with a great impact on physiological and pathological conditions. A derangement of intestinal microbiota may lead to microbial translocation of bacteria or their products in the liver, where endotoxins trigger inflammation, and hepatocellular damage, which in turn plays a key role in the development of HCC. The following liver injury and hepatocellular necrosis can promote the activation of a secondary proliferative pathway involving the hepatic progenitor cells (HPCs), a bipotential cell compartment that seems to contribute to hepatocarcinogenesis. Conclusion: The aim of this chapter is to summarize current knowledge on the potential role of intestinal microbiota in the pathogenesis of NAFLD and the subsequent development of HCC.

Intestinal Microbiota, Nonalcoholic Steatohepatitis and Hepatocellular Carcinoma: The Potential Role of Dysbiosis in the Hepatocarcinogenesis