GLP-1(7-36) Acetate is a major intestinal hormone that stimulates glucose-induced insulin secretion from β cells.

Cells exposed to phorbol 12-myristate 13-acetate for 2 hours exhibited significantly enhanced GLP-1(7-36) levels compared to untreated controls. Similarly, glucose exposure augmented GLP-1 secretion in a dose-responsive manner. Fatty acids, including palmitic, oleic, linoleic, and linolenic acids, also elevated GLP-1 secretion dose-dependently, with unsaturated fatty acids (oleic, linoleic, and linolenic acids) proving more potent than saturated palmitic acid. Furthermore, treatment with CPE on NCI-H716 cells led to a dose-dependent increase in GLP-1 levels, with a notable 37% rise at 0.1% CPE concentration[1].

Administering glucose via the stomach elevates active GLP-1(7-36) amide levels in portal blood within 10 minutes, showing a significant reduction at 30 minutes. Similarly, gastric TO administration also boosts active GLP-1 levels at 10 minutes, with levels returning to baseline at 60 minutes. Both glucose and TO independently enhance GLP-1 secretion in a dose-responsive manner, with their combined administration synergistically elevating peak GLP-1 concentrations. Mice treated with CPE exhibit increased active GLP-1 levels at 10 and 30 minutes compared to control mice. Additionally, CPE treatment results in slightly elevated levels of both active GLP-1 and insulin in portal blood post-glucose administration versus controls. Mice fed a high-fat diet, specifically C57BL/6J strain, exhibit hyperglycemia and diminished glucose tolerance[1].