What is the Origin of Glucose-Dependent Insulinotropic Polypeptide (GIP)?

GIP was initially discovered in the 1970s and named for its ability to inhibit gastric acid secretion, hence its original name, Gastric Inhibitory Peptide. However, subsequent research identified its far more potent role as a stimulator of insulin secretion following oral glucose ingestion. The name was officially revised to Glucose-Dependent Insulinotropic Polypeptide to reflect its principal and most significant function in glucose homeostasis.

What is the Mechanism of Glucose-Dependent Insulinotropic Polypeptide (GIP)?

Following the ingestion of carbohydrates and fats, GIP is rapidly secreted into the circulation. It binds to the GIP receptor, a G-protein-coupled receptor, on the pancreatic beta cells. This binding initiates an intracellular signaling cascade that increases the synthesis and secretion of insulin. Crucially, this effect is dependent on a high glucose concentration, ensuring that GIP only potentiates insulin release when it is physiologically needed to clear a meal-derived glucose load.

Glucose-Dependent Insulinotropic Polypeptide (GIP) ∞ Area

Glucose-Dependent Insulinotropic Polypeptide (GIP)

Meaning

Glucose-Dependent Insulinotropic Polypeptide (GIP) is a key incretin hormone, a member of the secretin family of peptides, secreted by the enteroendocrine K-cells predominantly located in the duodenum and jejunum of the small intestine. Its primary physiological role is to significantly amplify the release of insulin from the pancreatic beta cells, but only in the presence of elevated blood glucose concentrations. GIP is an essential component of the enteroinsular axis, mediating the phenomenon known as the incretin effect. This hormone is a major target for therapeutic strategies in type 2 diabetes.