GIPR is a G protein-coupled receptor that binds glucose-dependent insulinotropic polypeptide (GIP) and activates adenylyl cyclase signaling 1. As an incretin hormone receptor, GIPR mediates meal-stimulated insulin secretion and regulates glucagon secretion through direct actions on pancreatic islet β-cells 2. Beyond the pancreas, GIPR is widely expressed in metabolically relevant tissues including adipose tissue, liver, muscle, brain, and the cardiovascular system 3. In adipose tissue, GIPR agonism cooperates with insulin to enhance glucose uptake and lipid clearance in the fed state, while promoting lipolysis during fasting 4. GIPR activation in the central nervous system produces anorectic effects that reduce food intake and promote weight loss 3. Therapeutically, GIPR agonism via tirzepatide (a dual GIPR/GLP-1R co-agonist) reduces HbA1c and body weight more effectively than selective GLP-1R agonists 1, while GIPR antagonism combined with GLP-1R agonism (AMG-133) also promotes weight loss 5. Rare loss-of-function variants in GIPR are associated with lower BMI and reduced obesity risk, suggesting GIPR inhibition may provide therapeutic benefit 6. GIPR modulation represents a therapeutic target for type 2 diabetes, obesity, and related metabolic disorders 7.