Violeta B. Popov

TL;DR: It is demonstrated that the beneficial effects of DNP on hypertriglyceridemia, fatty liver, and insulin resistance can be dissociated from systemic toxicities and suggested the potential utility of liver-targeted mitochondrial uncoupling agents for the treatment of hypertrigenic fatty liver disease, NAFLD, metabolic syndrome, and T2D.

TL;DR: It is demonstrated that increase plasma APOC3 concentrations predispose mice to diet‐induced NAFLD and hepatic insulin resistance.

TL;DR: In Sprague Dawley rats fed an unsaturated fat diet, T2 administration failed to improve NAFLD or whole body insulin sensitivity, and there was a modest improvement in hepatic insulin signaling, but this was not associated with significant differences in hepatics insulin action.

TL;DR: Reducing β‐catenin expression decreases expression of enzymes involved in hepatic fatty acid esterification, ameliorates hepatic steatosis and lipid‐induced insulin resistance and Second‐generation antisense oligonucleotides against β‐Catenin protect mice against diet‐induced liver failure and hepatic and peripheral insulin resistance.

TL;DR: Insulin resistance (IR) plays a central role in the pathogenesis of these conditions via its relationship with CHC infection and appears to represent a negative predictor for antiviral response to pegylated interferon (IFN plus ribavirin), as manifested by lower sustained virological response rates.