Although peroxisome proliferator receptor (PPAR)-${alpha}$ and PPAR-${gamma}$ agonist have been developed as chemical tools to uncover biological roles for the PPARs such as lipid and carbohydrate metabolism, PPAR-${delta}$ has not been fully investigated. In this study, we examined the effects of the PPAR-${delta}$ agonist GW0742 on fatty liver changes and inflammatory markers. We investigated the effects of PPAR-${delta}$ agonist GW0742 on fatty liver changes in OLETF rats. Intrahepatic triglyceride contents and expression of inflammatory cytokines such as tumor necrosis factor-${alpha}$ (TNF-${alpha}$) and monocyte chemo-attractant protein-1 (MCP-1) and also, PPAR-${gamma}$ coactivator (PGC)-$1{alpha}$ gene were evaluated in liver tissues of OLETF rats and HepG2 cells after GW0742 treatment. The level of TNF-${alpha}$ and MCP-1 was also examined in supernatant of Raw264. 7 cell culture. To address the effects of GW0742 on insulin signaling, we performed in vitro study with AML12 mouse hepatocytes. Rats treated with GW0742 (10 mg/kg/day) from 26 to 36 weeks showed improvement in fatty infiltration of the liver. In liver tissues, mRNA expressions of TNF-${alpha}$, MCP-1, and PGC-$1{alpha}$ were significantly decreased in diabetic rats treated with GW0742 compared to diabetic control rats. We also observed that GW0742 had inhibitory effects on palmitic acid-induced fatty accumulation and inflammatory markers in HepG2 and Raw264.7 cells. The expression level of Akt and IRS-1 was significantly increased by treatment with GW0742. The PPAR-${delta}$ agonist may attenuate hepatic fat accumulation through anti-inflammatory mechanism, reducing hepatic PGC-$1{alpha}$ gene expression, and improvement of insulin signaling.