Particularly relevant is the finding that male Ldlr-/- mice fed the WD results in a NASH phenotype that recapitulates many of the phenotypic features seen in human NASH patients, including obesity, dyslipidemia, hyperglycemia, hepatic damage, hepatosteatosis, and the induction of multiple markers of inflammation, oxidative stress and fibrosis [29, 31]. This evidence concerns the gene LDLR and metabolic syndrome.