DPP4 and Insulin resistance: However, both lipogenesis and oleic acid uptake were similar in both control and DPP4 overexpressing hepatocytes,135 and genetic elimination of Dpp4 specifically from hepatocytes did not lead to any changes in NEFA, TG, or liver lipid accumulation.26 These data suggest aberrant communication between adipose tissue and the liver can be the main driver of DPP4’s role in insulin resistance and inflammation.