GLP-1 (Glucagon like peptide 1) is part of the group of incretin hormones that are secreted by the gastrointestinal tract in response to food intake to assist glucose stimulated insulin secretion and glucagon suppression. GLP-1 is a 30 aminoacid peptide cleaved from proglucagon and released by the L-cells of the distal ileum.  The intracellular precursor of GLP-1 (1-37) is cleaved to form the active peptides GLP-1 (7-37) and GLP-1 (7-36)NH₂.  The active peptides bind to the GLP-1 receptor (GLP-1r) expressed in the pancreatic beta cell and are quickly metabolized by the enzyme dipeptidyl peptidase IV (DPP-IV) to form the peptide GLP-1 (9-36), which has no insulin stimulating activity.  Binding of active GLP-1 to the receptor, increases cAMP levels and potentiates insulin secretion via Protein Kinase A (PKA) and the cAMP-regulated nucleotide exchange factor (Epac2). GLP-1 and its receptor are also suggested to play a role in the central nervous systems as mediators of satiety.  Intracerebroventricular GLP-1 has been shown to induce c-FOS activity in the hypothalamus and the central nucleus of the amygdala, both of which are important in the regulation of appetite. 

The role of GLP-1 in chronic diseases is controversial. Patients with type-II diabetes as well as morbidly obese subjects have been shown to have lower secretion of post-prandial GLP-1, which improves with treatment or weight loss.  Due to the beneficial effects of active GLP-1 as well as GLP-1r agonists in metabolic diseases, GLP-1 has been proposed to be an effective therapeutic approach to lowering glycemic levels and decreasing body fat content.  Furthermore, GLP-1 has been found to be cardioprotective during acute myocardial infarction.  In contrast with the GLP-1 protective findings, circulating GLP-1 has also been found to positively correlate with serum triclycerides and high levels are significantly associated with coronary plaque burden in patients receiving coronary CT-angiography.