Glucose-dependent insulinotropic polypeptide receptor and Glucagon-like peptide-1 receptor (GIP receptor (GIPR) and GLP-1 receptor (GLP-1R))

The Glucose-dependent insulinotropic polypeptide receptor and Glucagon-like peptide-1 receptor are both class B G protein-coupled receptors predominantly expressed in pancreatic β cells and other tissues, mediating the effects of their respective incretin hormones (GIP and GLP-1). These receptors are critical for the regulation of insulin secretion following nutrient ingestion, modulation of glucagon release, and, in the case of GLP-1R, control of appetite and body weight. Therapeutic agents targeting these receptors, particularly agonists, have revolutionized the management of type 2 diabetes and obesity, with several drugs marketed for these indications. Recently, dual agonists that engage both GIPR and GLP-1R have shown enhanced metabolic benefits. Both receptors are scientifically and medically well-defined targets, but they should be distinguished in records and databases as separate entities for clarity and specificity[1][2][3][4][5].

Other names

GIPRGastric inhibitory polypeptide receptorGIP receptorGLP-1RGLP1RGlucagon-like peptide-1 receptorGLP-1 receptor

Agonism at GIPR and GLP-1R promotes insulin release in a glucose-dependent manner. Suppression of glucagon secretion (mostly GLP-1R). Deceleration of gastric emptying (mostly GLP-1R). Increase in β-cell mass and survival (mainly GLP-1R). Appetite reduction and weight loss (GLP-1R).