Cholecystokinin-Pancreozymin Peptides

Introduction

Cholecystokinin-pancreozymin peptides, also named as cholecystokinin (CCK) or pancreozymin, is a brain-gut peptide secreted by the enteroendocrine cells and brain neurons of the duodenum and proximal jejunum. Cholecystokinin-pancreozymin peptides are involved in a wide range of physiological processes in the body, including digestion, satisfaction, anxiety, pain, and lordosis. In the current study, CCKs are known to be diverse. The main role of CCK-33 in the intestine is to stimulate the secretion of the pancreas, cause gallbladder contraction, enhance the movement of the small intestine and colon, inhibit gastric emptying, inhibit gastric acid secretion, relax the Oddi sphincter, and promote the growth of the pancreatic exocrine. Cholecystokinin in the central nervous system is involved in the most widespread neurotransmitter that inhibits feeding, anxiety, analgesia, and regulation of heart rate.

Mechanism of action

Cholecystokinin-pancreozymin peptides mainly have a relationship with cholecystokinin receptor (CCKR), and studies have shown that CCKR belongs to G-protein coupled receptor (GPCRs), a-type rhodopsin-like receptors. They have the functions of regulating pancreatic enzyme secretion and stimulating the contraction of the gallbladder to release bile. Cholecystokinin-pancreozymin peptides are a kind of endogenous neuroprotective factor and are important substances involved in neuroprotection and repair. Cholecystokinin-pancreozymin peptides and opioid peptide receptors overlap in the central nervous system, and their physiological interactions interact and can be activated under stress.

Application of Cholecystokinin-pancreozymin Peptides

Cholecystokinin-pancreozymin peptides have a growth effect on human tumors. Studies have shown that in many tumors, the growth of gastrin-related peptides is mediated by the receptor CCKR. Cholecystokinin-pancreozymin peptides help to find specific tumor therapeutic targets and design drugs for unique targets. Furthermore, it opens up broad prospects for the treatment of human gastrointestinal cancer and mental and neurological diseases.

Reference

1. Sonne, D.P., Rehfeld, J.F., Holst, J.J., et al. (2014) Postprandial gallbladder emptying in patients with type 2 diabetes: potential implications for bile-induced secretion of glucagon-like peptide 1. Eur J Endocrinol, 171(4): 407-419.