Furthermore, the liver could be in danger from microbial disorders and increased intestinal permeability, which may exacerbate the inflammatory responses to the nonalcoholic fatty liver [56]; research has shown that OA could treat nonalcoholic fatty liver by ameliorating intestinal barrier dysfunction and the Toll-like receptor 4 (TLR4)-associated inflammatory responses [57]. This evidence concerns the gene TLR4 and non-alcoholic fatty liver.