It has multiple actions including: potentiation of glucose-mediated insulin secretion mechanisms identified: increased -cell proliferation, resulting in an increase -cell mass (Fusco et al, 2017) stimulation of insulin biosynthesis at the translational level, helping to maintain -cell insulin stores and secretory capacity (Baggio & Drucker, 2007) because the GLP-1 effect is glucose-dependent (there is more insulin release when glucose levels are elevated, but less effect when glucose levels are normal), GLP-1 agonists have a lower risk for producing hypoglycemia compared to sulfonylureas (that chronically stimulate insulin release, independent of glucose concentration) suppression of postprandial glucagon release Evidence indicates that stimulation of pancreatic cells by GLP-1 increases their glucose sensitivity, resulting in less glucagon release at any glucose level (Baggio & Drucker, 2007)
187 Ruiz-DurntezE.Ruiz-OrtegaJ
Let's take a closer look at each option, as they each have their own advantages and considerations
[10] [39] [40] This led to the development of the first radioimmunoassay for detecting glucagon, described by Roger Unger's group in 1959
Additionally, it increases beta-adrenergic receptor expression, enhancing fat breakdown sensitivity, making it a promising candidate for obesity treatment (2)