In this study, using a combination of molecular, biochemical, biophysical, and bioinformatics approaches, we provide evidence for an additional novel mechanism by which XN and its derivative, TXN, can inhibit diet-induced hepatic steatosis through downregulation of hepatic FA uptake and lipid storage by binding to PPARγ in the liver and effectively antagonizing its actions. Here, PPARG is linked to Hepatic steatosis.