Abstract

Hepatocellular carcinoma (HCC) is the most prevalent type of primary liver cancer, the fifth most common type of solid tumor, and the third highest cause of cancer mortality worldwide (Parkin et al., 2005, Motola-Kuba et al., 2006). On the other hand, nonalcoholic fatty liver disease (NAFLD) is now recognized as one of the most common liver disorders (Lazo and Clark, 2008). The subclinical nature of this disease has prompted research to improve its diagnosis and prevent its progression to nonalcoholic steatohepatitis (NASH), liver cirrhosis, and HCC. An increasing number of reports indicate that NAFLD is the key link between obesity and HCC (Chavez-Tapia et al., 2009, Mendez-Sanchez et al., 2007). It has been suggested that most cases of HCC involve progression of NASH to cirrhosis (Caldwell et al., 2004). In 1980, Ludwig et al. described NASH as an advanced form of fatty liver disease. They defined it as a well-recognized clinical pathological syndrome that occurs primarily in obese women with diabetes mellitus and has histological similarities to alcoholic liver disease in the absence of heavy alcohol consumption (Ludwig et al., 1980). Some reports suggest that 10–24% of the populations of various countries have NAFLD. The prevalence of NAFLD is higher among obese and diabetic patients (70–86%). NASH is estimated to occur in 10% of NAFLD patients. NASH has been posited as a possible cause of cryptogenic cirrhosis (CC) (Bellentani et al., 2000). Patients with CC also develop HCC (Caldwell et al., 1999). In this review, we discuss the associations between obesity and cancer, between metabolic syndrome and NAFLD, and between NAFLD and HCC.

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