Hepatic lipid overloading mainly in the form of triglycerides is considered a prerequisite for
the development of nonalcoholic fatty liver disease (NAFLD). However, triglyceride
accumulation in the liver in response to lipid overflow may represent a protective mechanism
against lipotoxicity. Our aims were to assess the fundamental cellular mechanisms that link
lipid compartmentation in hepatocytes to liver damage and disease progression in NAFLD
by using both in vivo dietary models of NAFLD and in vitro cell models of lipid overloading …