liver modifications: hepatic inflammation, steatosis, and fibrosis, leading to increased risk of nonalcoholic fatty liver disease, increased triglyceride accumulation and lipogenesis, enhanced proinflammatory cytokine and serum insulin expression, and premature gluconeogenic gene activation with impaired carbohydrate metabolism [80,82,89]; 4. This evidence concerns the gene INS and metabolic dysfunction-associated steatotic liver disease.