Orlistat inhibits gastric, pancreatic, and carboxyl ester lipases, preventing the hydrolysis of triglycerides to free fatty acids and monoglycerides, and as such is widely used to treat obesity. With a 120 mg dose before each meal in healthy subjects, orlistat is reported to accelerate gastric emptying and attenuates the secretion of glucose-dependent insulinotropic peptide without affecting plasma responses of cholecystokinin, glucagon-like peptide-1, pancreatic polypeptide, or insulin.  It also targets additional serine hydrolases in the nervous system, such as diacylglycerol lipase (DAGL), which is responsible for the conversion of DAG to 2-AG. Orlistat potently inhibits human recombinant DAGLα with an IC50 value of 60 nM and at 1 µM inhibits the formation of 2-AG in intact cells in vitro.