Oxidative stress rather than triglyceride accumulation is a determinant of mitochondrial dysfunction in <i>in vitro</i> models of hepatic cellular steatosis

Abstract

Our data indicate that ROS formation, rather than cellular steatosis per se, impairs mitochondrial function. Thus, reduction in cellular steatosis may not always be the desired outcome without concomitant improvement in mitochondrial function and/or reducing of ROS formation.