In humans this is further supported by the observation of increased levels of TLR4 expression in hepatic tissue and increased plasma endotoxin presence in individuals with NAFLD and increased fructose intake in their diet, which may be explained by an increased permeability of the intestinal wall to endotoxin, stimulating increased TLR4 expression and activation (Thuy et al., 2008). This evidence concerns the gene TLR4 and metabolic dysfunction-associated steatotic liver disease.