LPL and Hepatic steatosis: Consistent with this finding, we found that SFZYD treatment induced similar significant decreases in the mRNA expression levels of PPARγ and its target genes, Lpl and Fabp4. Hepatic PPARγ is the main regulator of lipogenesis, fatty acid metabolism, and glucose metabolism and promotes lipid storage [21, 22]; thus, SFZYD-mediated regulation of the PPARγ gene may underlie the effects of SFZYD in liver steatosis.