Glucose-dependent insulinotropic polypeptideGIP
The second incretin, with distinct adipose and CNS biology.
Identity
- Class
- Incretin peptide (42 aa)
- Source
- Intestinal K-cells (duodenum/jejunum)
- Receptor
- GIP receptor (GIPR), a class B GPCR
Key properties
Molecular weight
~4,983.6 Da
Approximate values for the native hormone. Engineered analogs are often deliberately larger and far longer-acting.
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.
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