Moreover, de novo lipogenesis is increased due to the constant high levels of insulin, producing even more triglycerides and further enhancing hepatic gluconeogenesis17,18 Thus, hepatic insulin resistance in individuals with NAFLD is considered to be limited to the pathway involving suppression of hepatic glucose production and not the lipogenic pathway, which is referred to as selective insulin resistanc.19 Here, INS is linked to metabolic dysfunction-associated steatotic liver disease.