Insulin resistance and poor glycemic control are key drivers of the development of non-alcoholic fatty liver disease (NAFLD) and have recently been shown to be associated with fibrosis progression in nonalcoholic steatohepatitis (NASH). The authors set out to determine whether Protease-activated receptor 2 (PAR2), a sensor of extracellular inflammatory and coagulation proteases, links NAFLD and NASH with liver glucose metabolism.
