Glucose-dependent insulinotropic peptide receptor (GIPR) (GIPR)

The Glucose-dependent insulinotropic peptide receptor (GIPR) is a member of the Class B G protein-coupled receptor family, primarily expressed in pancreatic beta cells, adipose tissue, and the central nervous system [1, 5]. Its primary biological function is to mediate the effects of GIP, an incretin hormone that stimulates insulin secretion from the pancreas in a glucose-dependent manner, thereby reducing postprandial blood glucose levels without significant risk of hypoglycemia [3]. Beyond its insulinotropic effects, GIPR signaling plays a role in lipid metabolism, adipocyte function, and bone formation [2, 5]. In clinical medicine, GIPR has emerged as a major therapeutic target for the treatment of Type 2 diabetes and obesity [4]. Modern drugs, such as the dual GIPR and GLP-1R agonist Tirzepatide, leverage GIPR activation to enhance weight loss and glycemic control beyond what is achievable with GLP-1R mono-agonists [4]. While generally well-tolerated, the primary safety concerns associated with GIPR-targeting therapies include gastrointestinal side effects such as nausea and vomiting [3, 4]. Sources: [1] UniProt (P48546) [2] NCBI Gene (ID: 2696) [3] StatPearls: Physiology, Incretin Hormones [4] NEJM: Tirzepatide once weekly for the treatment of obesity [5] IUPHAR/BPS Guide to Pharmacology: GIP receptor

Other names

Gastric inhibitory polypeptide receptorGIP receptorGIP-R

Agonism of the G protein-coupled receptor to stimulate adenylate cyclase, increasing intracellular cAMP and triggering glucose-dependent insulin secretion [1, 3, 5].