What is Glucose-dependent insulinotropic polypeptide (GIP)?

The second incretin, with distinct adipose and CNS biology. Structurally it is Incretin peptide (42 aa).

How strong is the evidence for GIP?

PeptideHormone grades GIP 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 GIP?

The reported circulating half-life of GIP is ~5–7 min (native; DPP-4).

Glucose-dependent insulinotropic polypeptideGIP

The second incretin, with distinct adipose and CNS biology.

EndogenousEstablishedCompare lineage

The body rarely says anything important only once. GIP is the second voice in the incretin conversation, and the one still being argued over.

Identity

Class: Incretin peptide (42 aa)
Source: Intestinal K-cells (duodenum/jejunum)
Receptor: GIP receptor (GIPR), a class B GPCR

Key properties

Evidence floorClinicalREF1CLIN1

Molecular weight

~4,983.6 Da

REF

Half-life (native)

~5–7 min (native; DPP-4)

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

GIP is secreted from K-cells after a meal and, like GLP-1, potentiates glucose-dependent insulin release. Beyond the islet it has actions on adipose tissue and the CNS that differ from GLP-1, which is why GIP/GLP-1 co-agonism is studied for effects neither achieves alone.

Reference notes

GIP's adipose and central actions are an area of active investigation and debate.
The incretin effect — far more insulin from oral than IV glucose — reflects combined GLP-1 and GIP signaling.
Whether GIPR agonism or antagonism is metabolically preferable is not fully settled.

Common questions

What is Glucose-dependent insulinotropic polypeptide (GIP)?: The second incretin, with distinct adipose and CNS biology. Structurally it is Incretin peptide (42 aa).
How does GIP work?: GIP is secreted from K-cells after a meal and, like GLP-1, potentiates glucose-dependent insulin release. Beyond the islet it has actions on adipose tissue and the CNS that differ from GLP-1, which is why GIP/GLP-1 co-agonism is studied for effects neither achieves alone.
How strong is the evidence for GIP?: PeptideHormone grades GIP 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 GIP?: The reported circulating half-life of GIP is ~5–7 min (native; DPP-4).

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.Glucose-dependent insulinotropic polypeptide (GIP) · Molecular metabolism, 2025 · PMID 40024571
2.Mechanisms of action and therapeutic applications of GLP-1 and dual GIP/GLP-1 receptor agonists · Frontiers in endocrinology, 2024 · PMID 39114288

External references

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