The pathogenesis of nonalcoholic steatohepatitis is multifactorial, involving steatosis, lipotoxicity, hepatic inflammation, and fibrosis. The present studies show that acetyl-CoA carboxylase inhibition produces direct improvements in hepatic steatosis, inflammation, and fibrosis in both primary human cell systems and rodent nonalcoholic fatty liver disease/nonalcoholic steatohepatitis models.
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