Scientific Glossary

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GLP-1 is released from the gut after meals and exerts multiple metabolic effects: stimulates glucose-dependent insulin secretion from pancreatic beta-cells, suppresses glucagon from alpha-cells, slows gastric emptying (creating satiety), and acts centrally to reduce appetite. GLP-1 has a very short endogenous half-life (~2 minutes) due to DPP-4 degradation. Pharmaceutical GLP-1 receptor agonists are engineered for much longer half-lives (days to weeks).

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GIP is the other major incretin hormone. Like GLP-1, it stimulates insulin secretion in response to blood glucose elevation. However, GIP receptors are also expressed in adipose tissue and bone. The GIP receptor's role in fat metabolism is complex — it may promote fat storage in some contexts. Dual GIP/GLP-1 receptor agonists (like tirzepatide) leverage both pathways, potentially explaining their superior weight reduction vs. GLP-1 monotherapy.

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The two main incretins are GLP-1 (from L-cells) and GIP (from K-cells). The incretin effect accounts for 50-70% of postprandial insulin secretion in healthy individuals — explaining why oral glucose produces more insulin than IV glucose (the "incretin effect"). This glucose-dependence is therapeutically important: incretins only stimulate insulin when blood glucose is elevated, dramatically reducing hypoglycemia risk vs. sulfonylureas. Incretin-based therapies (GLP-1RAs, DPP-4 inhibitors, dual/triple agonists) are now foundational to metabolic disease research.