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CCK-8表现出各种胃肠道作用，如胆囊收缩、胰腺分泌和胃肠道转运刺激。在大鼠中，CCK-8促进了瘦素从外周循环到脑脊液的摄取及其进入下丘脑。

CCK-8 exhibits various gastrointestinal effects as contraction of the gallbladder and stimulation of pancreatic secretion and gastrointestinal transit. In rats, CCK-8 facilitated the uptake of leptin from peripheral circulation to cerebrospinal fluid and its access to the hypothalamus.

CCK-Octapeptide (26-33) (Sulfated Form) is a peptide that has been shown to have a variety of biological effects. It has been found to enhance the activity of rifampicin against tuberculosis by increasing the activity of the kinase protein. CCK-Octapeptide (26-33) (Sulfated Form) also has natriuretic peptide-like activity, which means it can regulate blood pressure and fluid balance in the body. In addition, it has been shown to inhibit tumor growth and metastasis in animal models, possibly through its ability to modulate guanosine triphosphate-binding proteins. CCK-Octapeptide (26-33) (Sulfated Form) also exhibits trypsin inhibitory activity and thymidine uptake inhibition. Furthermore, it has been studied as a potential treatment for cancer and as an alternative to vasopressin or nesiritide in certain medical conditions where natriuretic peptides are used ther

Definition

Cholecystokinin (CCK), also called pancreozymin, is a peptide hormone in the small intestine that constitutes the classical gut hormone triad together with gastrin and secretin1. CCK is secreted into the blood following ingestion of a meal and plays a critical role in the ingestion, absorption, intestinal motility, satiety signaling, inhibition of gastric acid secretion and digestion of food1.

Discovery

CCK was discovered in 1928 because of its ability to induce gallbladder contraction2.

Classification

CCK is a neuropeptide.  It is a family of hormones identified by the number of amino acids, for eg: CCK58 and CCK331. 

Structural Characteristics

Prepro-CCK is a115 amino acid peptide that is first cleaved to pro-CCK which in turn results in CCK58, the major processed form of CCK3.  CCK58 assumes a helix-turn-helix configuration3.

Mode of action

CCK binds to CCK receptors on the cell membrane that when activated increase the turnover of phosphatidyl inositol which results in the release of intracellular calcium4.  The calcium released causes increased enzyme secretion either directly or through activation of protein kinase C4.

Functions

CCK induces the gall bladder to contract and eject bile into the intestine5. It stimulates the acinar cells of the pancreas to release water and ions and stimulates the secretion of a juice rich in pancreatic digestive enzymes5. It is known to induce growth of the exocrine pancreas and to stimulate insulin secretion5. CCK is the most abundant neuropeptide in the human brain where it induces panic attacks that are antagonized by a central cholecystokinin receptor antagonist6. ProCCK is expressed in certain neuroendocrine tumors and sarcomas, and the secretion of CCK is impaired in celiac disease and bulimia nervosa7.

References

1.     Fink H, Rex A, Voits M, Voigt JP (1998). Major biological actions of CCK--a critical evaluation of research findings. Exp Brain Res., 123 (1-2), 77–83.

2.     Hunt, J. N. (1948). A method for estimating peptic activity in gastric contents. Biochem. J., 42, 104-109.

3.     Book: Neuropeptides By Fleur L. Strand, 387-389.

4.     Dufresne M, Seva C, Fourmy D (2006). Cholecystokinin and gastrin receptors. Physiol. Rev., 86 (3), 805–47.

5.     Chandra R, Liddle RA (2007). Cholecystokinin. Curr Opin Endocrinol Diabetes Obes., 14(1), 63-7.

6.     Rehfeld JF, Friis-Hansen L, Goetze JP, Hansen TV (2007). The biology of cholecystokinin and gastrin peptides. Curr Top Med Chem, 7(12), 1154-65.

7.     Rehfeld JF (2004). Clinical endocrinology and metabolism. Cholecystokinin. Best Pract Res Clin Endocrinol Metab., 18(4), 569-86.