Cholecystokinin
The original satiety signal — a gut-brain peptide that tells you to stop eating, stimulates digestion, and modulates anxiety and pain in the CNS.
A family of gut-brain peptides (CCK-8 through CCK-58) released by I-cells of the duodenum after a meal that reduce food intake via vagal CCK1 receptors, stimulate gallbladder contraction and pancreatic enzyme secretion, and act as an anxiogenic neuropeptide in the brain via CCK2 receptors.
Mechanism of action
Binds CCK1R (peripheral gut — mediates satiety, gallbladder contraction, pancreatic enzyme secretion) and CCK2R (primarily CNS — modulates anxiety, pain perception, and memory). CCK1R activation on vagal afferents transmits the satiety signal to the nucleus tractus solitarius.
Primary uses
- Endogenous post-meal satiety signaling
- Gallbladder contraction and pancreatic enzyme secretion
- CNS neuropeptide (anxiety modulation, pain perception)
- Diagnostic use: sincalide for gallbladder function testing
Typical dosing
Sincalide 0.02 mcg/kg IV is used diagnostically for cholecystography. Not used therapeutically for satiety.
Regulatory status
Sincalide (Kinevac, a synthetic CCK-8 analog) is FDA-approved as a diagnostic agent for gallbladder contraction studies and pancreatic function testing, but not as a therapeutic.
References
- [pubmed] Gibbs J, Young RC, Smith GP. "Cholecystokinin decreases food intake in rats." J Comp Physiol Psychol. 1973;84(3):488-495.
- [review] Rehfeld JF. "Cholecystokinin -- from local gut hormone to ubiquitous messenger." Front Endocrinol. 2017;8:47.
Related peptides
This entry is for educational purposes only and does not constitute medical advice. Dosing information reflects published regulatory or research data and is not a recommendation. Many compounds described here are not approved for human use in the United States. Consult a licensed medical professional before considering any peptide therapy.