The etiology of non-alcoholic steatohepatitis (NASH) has been complicated. An increasing body of literature has indicated that hepatic oxidative stress exerts a causal role in driving NASH. Neverthele
Two-month-old C57BL/6J male mice were placed on chow diet or a diet enriched in high fat, cholesterol, and fructose (Research diet D09100301: 40 kcal% fat, 2% cholesterol, 20 kcal% fructose, HFCF diet
We investigated the biological function of INSIG1 in acute (CCl4) and chronic (NASH) liver damage. Male whole-body Insig1 wild-type (WT), Heterozygous (HET) and Knock-out (KO) mice were: 1) challenged
The liver is undergoing major rearrangements during the development of non-alcoholic steatohepatitis (NASH), from steatosis to severe lipid accumulation, inflammation and fibrosis. The mechanisms for
