CholecystokininCCK

Triggers gallbladder contraction, pancreatic enzymes, and satiety.

EndogenousEstablished

Identity

Class: Gut peptide (multiple active lengths, e.g. CCK-8)
Source: Duodenal I-cells (and CNS neurons)
Receptor: CCK1 (gut) and CCK2 (CNS) receptors

Key properties

Molecular weight

≈ 1,143.3 Da

Half-life (native)

~1–2.5 min

Model dosing

Approximate values for the native hormone. Engineered analogs are often deliberately larger and far longer-acting.

Mechanism

Released in response to dietary fat and protein, CCK stimulates gallbladder contraction and pancreatic enzyme secretion and signals satiety. Its peripheral (CCK1) and central (CCK2) receptors separate its digestive and neural roles.

Reference notes

CCK couples nutrient sensing to the mechanics of digestion (bile and enzymes).
CCK1 vs CCK2 distribution splits its digestive and central effects.
It was one of the earliest gut peptides linked to meal-ending satiety.

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.Role of cholecystokinin in satiation: a systematic review and meta-analysis · The British journal of nutrition, 2023 · PMID 35152916
2.Cholecystokinin · Current opinion in endocrinology, diabetes, and obesity, 2007 · PMID 17940422