Progress in biophysics and molecular biologyAug 9, 2011

Comparison of two gut hormones, GLP-1 and GIP, in boosting insulin release and protecting insulin-producing cells

GLP-1 Therapies Weekly Brief ↗PubMed ↗DOI ↗

Updated Apr 2, 2026

Abstract

Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are key incretin hormones that stimulate insulin secretion from pancreatic β cells.

GIP and GLP-1 are secreted from the intestine in response to glucose or nutrient intake.
These hormones bind to specific receptors, GIP receptor (GIPR) and GLP-1 receptor (GLP-1R), activating intracellular cAMP in pancreatic β cells.
In addition to stimulating insulin secretion, GIP and GLP-1 may help preserve pancreatic β cell mass by reducing cell death and promoting cell growth.
Incretin-based therapies are becoming increasingly popular for the treatment of type 2 diabetes.
Despite extensive research, the exact molecular mechanisms by which GIPR and GLP-1R activation enhances glucose-dependent insulin secretion remain unclear.

Simplified

Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the two primary incretin hormones secreted from the intestine upon ingestion of glucose or nutrients to stimulate insulin secretion from pancreatic β cells. GIP and GLP-1 exert their effects by binding to their specific receptors, the GIP receptor (GIPR) and the GLP-1 receptor (GLP-1R), which belong to the G-protein coupled receptor family. Receptor binding activates and increases the level of intracellular cAMP in pancreatic β cells, thereby stimulating insulin secretion glucose-dependently. In addition to their insulinotropic effects, GIP and GLP-1 have been shown to preserve pancreatic β cell mass by inhibiting apoptosis of β cells and enhancing their proliferation. Due to such characteristics, incretin hormones have been gaining mush attention as attractive targets for treatment of type 2 diabetes, and indeed incretin-based therapeutics have been rapidly disseminated worldwide. However, despites of plethora of rigorous studies, molecular mechanisms underlying how GIPR and GLP-1R activation leads to enhancement of glucose-dependent insulin secretion are still largely unknown. Here, we summarize the similarities and differences of these two incretin hormones in secretion and metabolism, their insulinotropic actions and their effects on pancreatic β cell preservation. We then try to discuss potential of GLP-1 and GIP in treatment of type 2 diabetes.

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Comparison of two gut hormones, GLP-1 and GIP, in boosting insulin release and protecting insulin-producing cells

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