AR and metabolic dysfunction-associated steatotic liver disease: Our data suggest that inhibition of AR in the T2DM db/db mice led to significant activation in hepatic PPARα and significant reductions in serum triglycerides (TG) and hepatic TG, suggesting that under hyperglycemia, AR/the polyol pathway might be greatly upregulated to contribute significantly to the hepatic regulation of TG metabolism and the development of nonalcoholic steatohepatitis (NASH) or nonalcoholic fatty liver disease (NAFLD).