TLR4 and metabolic dysfunction-associated steatotic liver disease: Models of bacterial overgrowth have shown promise as an initiator of fatty liver and patients with NAFLD present with upper intestinal bacterial overgrowth and enhanced intestinal permeability [79, 80].Consistent with gut-derived endotoxin mediating these effects, TLR4-mutant mice showed reduced lipid accumulation following feeding a high-fructose diet or methionine-choline deficient diet when compared to their TLR4-wild type controls suggesting that LPS may contribute to disease progression [81, 82].