Regarding the roles of visceral adipose Ang II in the pathogenesis of fructose-induced metabolic syndrome, this study shows that high-fructose feeding increased visceral adipose Ang II expression, NOX isoforms expressions, oxidative stress (reducing SOD activity and increasing lipid peroxide levels), dysregulated adipocytokines, and visceral adiposity. This evidence concerns the gene SOD1 and metabolic syndrome.