GLP-1(7-36), amide TFA is a prominent intestinal hormone known to stimulate glucose-induced insulin secretion from β cells[1].

Cells treated with phorbol 12-myristate 13-acetate for 2 h has significantly higher active GLP-1(7-36) Acetate (Human GLP-1-(7-36)-amide Acetate) concentrations in the media than those in the control. The glucose treatment also increases active GLP-1 secretion from cells in dose-dependent manner. Palmitic, oleic, linoleic or linolenic acid dose-dependently stimulated active GLP-1 secretion from cells. Active GLP-1 secretion is significantly greater with unsaturated fatty acids such as oleic, linoleic and linolenic acids than with palmitic acid. The treatment of NCI-H716 cells with CPE dose-dependently increases active GLP-1 concentrations in the media. A 37% increase is observed in active GLP-1 secretion from these cells at a concentration of 0.1 % CPE[1].

Gastric administration of glucose increases active GLP-1(7-36) amide levels in the portal blood after 10 min, followed by a marked decrease at 30 min. The gastric administration of TO also increases active GLP-1 levels after 10 min, and followed by a decrease to basal levels at 60 min. Individually, glucose and TO increase the secretion of GLP-1 in a dose-dependent manner. Furthermore, the co-administration of glucose and TO additively increase peak GLP-1 levels. CPE-administered mice have higher active GLP-1 levels in the portal blood at 10 and 30 min than those in the control mice. When glucose is administered with CPE, active GLP-1 and insulin levels in the portal blood are slightly higher in CPE-administered mice than in the control mice. High-fat diet-fed C57BL/6J mice develop hyperglycaemia and impair glucose tolerance[1].