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Nonalcoholic steatohepatitis (NASH), occurs frequently with diabetes mellitus and obesity, contributes to insulin resistance, can develop cirrhosis or even hepatocellular carcinoma (HCC). Although NASH has become more common, its underlying mechanism is still not clear and effective therapy has not been established. Currently, it has been recognized that the multiple parallel factors, including genetic differences, insulin resistance, lipotoxicity and dysbiosis act synergistically in genetically in pathogenesis of NASH. Impaired autophagy parallel to excess lipid supply might explain the progression of NASH to HCC. Liver-specific knockout mice of phosphatase and tensin homolog deleted on chromosome ten (PTEN) develops steatohepatitis followed by HCC, suggesting a potential role for this molecule in development and progression of NASH.
Sumio Watanabe (Sun,) studied this question.