Objective: Unlike other GPR119 agonist, DA-1241 showed a long-term beneficial effect on glucose and lipid metabolism in previous studies. We investigated the anti-diabetes effect of DA-1241 in vitro and in vivo. We also studied hepatic autophagy, gluconeogenesis, and change in GLP-1 levels. Methods: We evaluated the effect of DA-1241 on gluconeogenic enzyme expression and autophagic flow in HepG2 cell and liver from LC3-GFPtransgenic mice. We treated DA-1241 to high fat diet (HFD) fed C57BL/6J mice for 16 weeks and measured serum insulin and GLP-1 during OGTT. We estimated insulin secretion with insulinogenic index. Also, we calculated Matsuda index for insulin resistance. Results: DA-1241 reduced gluconeogenic enzyme expression and blocked autophagic flow in HepG2 cell. DA-1241 initially induced autophagic activation then blocked autophagic flow in liver in LC3-GFP transgenic mice. Fasting blood glucose was decreased with DA-1241 treatment in HFD fed mice. DA-1241 treatment improved glucose tolerance with increased serum GLP-1 and insulin level. Insulinogenic index was improved with DA-1241 treatment. However, insulin tolerance was not improved with DA-1241 treatment as revealed by Matsuda index. Conclusion: DA-1241 reduced fasting blood glucose level via inhibition of gluconeogenesis in liver. This effect may be associated with autophagic process blockage. DA-1241 enhanced GLP-1 secretion and insulin secretion which resulted in improvement in glucose tolerance however insulin resistance was not changed.