As expected from studies investigating the actions resulting from administration of GLP-1, stimulation of the GLP-1 receptor directly with a GLP-1R agonist or indirectly with a DPP-4 inhibitor (by inhibiting enzymatic degradation of endogenous GLP-1) serves to increase insulin secretion in a glucose-dependent manner through direct activation of pancreatic islet β-cells [6-10] and to inhibit glucagon secretion in a glucose-dependent manner (ie., only during hyperglycemia) through direct activation of pancreatic islet α-cells [6,8,9,11-14]. This evidence concerns the gene GLP1R and Hyperglycemia.