Glossary
GIP
GIP is the second incretin hormone, secreted by duodenal K-cells. Its receptor biology, its signalling in fat tissue and its place in dual-agonist research.
GIP stands for glucose-dependent insulinotropic polypeptide (formerly gastric inhibitory polypeptide). It is a 42-amino-acid incretin released from K-cells of the duodenum and upper jejunum when nutrients — fat and glucose in particular — arrive. Together with GLP-1 it explains the incretin effect: oral glucose triggers a bigger insulin response than an intravenous load that produces the same blood glucose level.
The receptor and published findings
The GIP receptor is a class B GPCR located on pancreatic beta-cells, fat cells, bone and parts of the central nervous system. Studies report glucose-dependent enhancement of insulin secretion, influences on lipid handling and blood flow in adipose tissue, and central effects on food intake. How GIP affects energy balance has been truly controversial — in rodent models, both activating and blocking the receptor have been reported to lower body weight, and the mechanism is still unresolved. Just like GLP-1, native GIP is quickly cleaved by DPP-4.
Its role in dual agonists
GIP forms the second half of dual incretin pharmacology. Tirzepatide, a GIP/GLP-1 dual agonist, is built on a backbone derived from GIP — which is how GIP receptor biology went from a side note to a core subject of metabolic research.
Related terms
triple agonist · GLP-1 receptor agonist. See the GIP research family, Tirzepatide, and what tirzepatide is.