What is Glucagon-like peptide-1 (GLP-1)?

The incretin that anchors the modern metabolic toolkit. Structurally it is Proglucagon-derived peptide (~30–31 aa).

How strong is the evidence for GLP-1?

PeptideHormone grades GLP-1 at the "Established" evidence tier — its mechanism and core effects are settled across the peer-reviewed literature. It is catalogued as an endogenous signal the body produces itself, and the tier is an editorial judgment about the public literature that can change as the science does.

What is the half-life of GLP-1?

The reported circulating half-life of GLP-1 is ~1–2 min (native; DPP-4 cleaved).

Glucagon-like peptide-1GLP-1

The incretin that anchors the modern metabolic toolkit.

EndogenousEstablishedCompare lineage

Two minutes of life, and the whole modern metabolic class built to prolong them — the clearest case in biology of brevity being the design, not the flaw.

Identity

Class: Proglucagon-derived peptide (~30–31 aa)
Source: Intestinal L-cells (and some CNS neurons)
Receptor: GLP-1 receptor (GLP-1R), a class B GPCR

Key properties

Evidence floorClinicalREF1CLIN1

Molecular weight

~3,297.7 Da

REF

Half-life (native)

~1–2 min (native; DPP-4 cleaved)

CLIN

Model dosing

Approximate values for the native hormone; engineered analogs are often deliberately larger and far longer-acting. Each figure carries its own provenance tier, and the floor is the weakest of them - the Standard.

Mechanism

Released from gut L-cells in response to nutrients, GLP-1 binds GLP-1R on pancreatic beta cells to amplify glucose-dependent insulin secretion. It also slows gastric emptying and signals satiety centrally. Native GLP-1 is degraded within minutes by DPP-4, which is why long-acting receptor agonists are engineered for protease resistance.

Reference notes

Glucose-dependence is the safety crux: GLP-1 augments insulin only when glucose is elevated, limiting hypoglycemia risk relative to insulin secretagogues.
Co-agonism with GIP (and, in some candidates, glucagon) is an active design strategy aimed at additive metabolic effects.
The very short native half-life is the central pharmacological problem its agonists are built to solve.

Common questions

What is Glucagon-like peptide-1 (GLP-1)?: The incretin that anchors the modern metabolic toolkit. Structurally it is Proglucagon-derived peptide (~30–31 aa).
How does GLP-1 work?: Released from gut L-cells in response to nutrients, GLP-1 binds GLP-1R on pancreatic beta cells to amplify glucose-dependent insulin secretion. It also slows gastric emptying and signals satiety centrally. Native GLP-1 is degraded within minutes by DPP-4, which is why long-acting receptor agonists are engineered for protease resistance.
How strong is the evidence for GLP-1?: PeptideHormone grades GLP-1 at the "Established" evidence tier — its mechanism and core effects are settled across the peer-reviewed literature. It is catalogued as an endogenous signal the body produces itself, and the tier is an editorial judgment about the public literature that can change as the science does.
What is the half-life of GLP-1?: The reported circulating half-life of GLP-1 is ~1–2 min (native; DPP-4 cleaved).

Selected literature

Curated peer-reviewed reviews, sourced from PubMed. Selected for relevance, not exhaustive — open any entry on PubMed for the full record and its primary citations.

1.Mechanisms of Action and Therapeutic Application of Glucagon-like Peptide-1 · Cell metabolism, 2018 · PMID 29617641
2.The physiology of glucagon-like peptide 1 · Physiological reviews, 2007 · PMID 17928588
3.Glucagon-like peptide-1 receptor: mechanisms and advances in therapy · Signal transduction and targeted therapy, 2024 · PMID 39289339

External references

GLP-1 in the public knowledge graph — the same entity resolved across the authoritative chemistry and protein databases.