Abstract
Nonalcoholic fatty liver disease (NAFLD) primarily begins with hepatosteatosis, resulting in hepatocellular damage, inflammation, and fibrosis. Although hepatosteatosis per se is well tolerated and protects from cellular damage, convincing evidence shows that lipotoxicity drives the progression of simple steatosis to nonalcoholic steatohepatitis (NASH). Although how hepatosteatosis causes lipotoxicity is incompletely defined, the concept of “fat accumulation and lipotoxicity are not synonymous” suggests that the type of fatty acids (quality) determines NASH progression in addition to quantity.
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