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Pathway

Fullness hormone (CCK)

Cholecystokinin

The Meal-Ending Signal

1 blend on this site modulates it.

Also searched as Cholecystokinin.

In depth

Cholecystokinin — released by the upper small intestine when fat and protein arrive, it slows the stomach and tells the brain the meal is done.

What drives it

Gut-brain signal increases it.

Bitter taste receptors (T2Rs) comprise a family of 25 G protein-coupled receptors that are expressed in multiple tissues, including enteroendocrine cells (EECs), of the GI tract. 10.1093/ajcn/nqab418. doi 10.1093/ajcn/nqab418

Gut barrier increases it.

10.14814/phy2.70373 — exposure of cultured enteroendocrine cells to promiscuous bitter tastants (e.g. quinine) is known to increase intracellular calcium signaling and stimulate release of hormones, including cholecystokinin (CCK). 10.1093/ajcn/nqab418. doi 10.14814/phy2.70373

What it drives

It increases Curbs appetite.

PMC1382399 — Gut hormones such as cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) play a role as satiation factors. PMID 27875537 · PMC1382399

It reduces Stomach emptying.

PMC423501 — L-trp at the higher dose stimulates CCK release (p = 0.0018), and induces a significant retardation in gastric emptying (p = 0.0033) ... an effect that could be mediated by CCK. PMID 27875537 · PMC423501

It increases Pancreatic acinar cells.

CCK acts on acinar CCK-A receptors to trigger zymogen granule secretion; supramaximal CCK causes premature intracellular zymogen activation. PMID 40563241

Blends that modulate it

Each blend page names this pathway and carries the study behind its claim.

Appetite Suppressant (Hunger Signal Control) →

See it on the map

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