Technical Data

G2020-06
Grade
Highly Purified
EU Commodity Code
38220090
Shipping Temp
Blue Ice
Storage Temp
-20°C
Gastrin Tetrapeptide (human) (Gastrin (14-17), Cholecystokinin Tetrapeptide, CCK-4, Cholecystokinin Octapeptide (5-8))
Trp-Met-Asp-Phe-NH2

In humans, gastrin is a hormone that stimulates secretion of gastric acid (HCl) by the parietal cells of the stomach and aids in gastric motility. It is released by G cells in the stomach, duodenum, and the pancreas. Its existence was first suggested in 1905 by the British physiologist John Sydney Edkins,[1][2] and gastrins were isolated in 1964 by Gregory and Tracy in Liverpool.[3] The GAS gene is located on the long arm of the seventeenth chromosome (17q21).[4] Gastrin is a linear peptide hormone produced by G cells of the duodenum and in the pyloric antrum of the stomach. It is secreted into the bloodstream. Gastrin is found primarily in three forms: gastrin-34 ('big gastrin'), gastrin-17 ('little gastrin') and gastrin-14 ('minigastrin'). Also, pentagastrin, a five amino acid sequence artificially synthesized peptide, has a five amino acid sequence identical to the last five amino acid sequence at the C-terminus end of gastrin.

Gastrin is released in response to certain stimuli. These include: stomach distension, vagal stimulation (mediated by the neurocrine bombesin, or GRP in humans), the presence of partially digested proteins especially amino acids and hypercalcemia. Gastrin release is inhibited by the presence of acid (primarily the secreted HCl) in the stomach (a case of negative feedback) and Somatostatin, which inhibits the release of gastrin, along with secretin, GIP (gastroinhibitory peptide), VIP, glucagon and calcitonin.
The presence of gastrin stimulates parietal cells of the stomach to secrete hydrochloric acid (HCl)/gastric acid. This is done indirectly via binding onto CCK2/gastrin receptors on ECL cells in the stomach, which then responds by releasing histamine, which in turn acts in a paracrine manner on parietal cells stimulating them to secrete H+ ions. This is the major stimulus for acid secretion by parietal cells. Along with the above mentioned function, gastrin has been show to have additional functions as well: (i). Stimulates parietal cell maturation and fundal growth. (ii). Causes chief cells to secrete pepsinogen, the zymogen (inactive) form of the digestive enzyme pepsin. (iii). Increases antral muscle mobility and promotes stomach contractions. (iv) Strengthens antral contractions against the pylorus, and constricts the pyloric sphincter, which slows gastric emptying. (v). Plays a role in the relaxation of the ileocecal valve.[5] (vi). Induces pancreatic secretions and gallbladder emptying.[6] (vii). Impacts lower esophageal sphincter (LES) tone, causing it to relax.[7] Taking this into consideration, high levels of gastrin may play a role in the development of some of the more common LES disorders such as acid reflux disease.
In the Zollinger-Ellison syndrome, gastrin is produced at excessive levels, often by a gastrinoma (gastrin-producing tumor, mostly benign) of the duodenum or the pancreas. To investigate for hypergastrinemia (high blood levels of gastrin), a 'pentagastrin test' can be performed. In autoimmune gastritis, the immune system attacks the parietal cells leading to hypochlorhydria (low stomach acidity). This results in an elevated gastrin level in an attempt to compensate for low acidity. Eventually, all the parietal cells are lost and achlorhydria results leading to a loss of negative feedback on gastrin secretion.
Sequence (linear): Trp-Met-Asp-Phe-NH2
Storage and Stability
Lyophilized powder may be stored at 4°C for short-term only. Stable for 12 months at -20°C. Reconstitute to nominal volume (see reconstitution instructions for peptides) and store at -20°C. For maximum recovery of product, centrifuge the original vial prior to removing the cap. Further dilutions can be made in assay buffer.
Source
Synthetic peptide
Purity
95+%, HPLC, Mass Spec
Form
Supplied as a lyophilized powder.
Important Note
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications without the expressed written authorization of United States Biological.

Intended for research use only. Not for use in human, therapeutic, or diagnostic applications.

References
General References: |1. Edkins JS (13 Mar 1906). "The chemical mechanism of gastric secretion". J. Physiol. (Lond.) 34 (1-2): 133–44. PMID 16992839. PMC: 1465807.|2. Modlin IM, Kidd M, Marks IN, Tang LH (1997). "The pivotal role of John S. Edkins in the discovery of gastrin". World J Surg 21 (2): 226–34. doi:10.1007/s002689900221. PMID 8995084.|3. Gregory RA, Tracy HJ (1964). "The constitution and properties of two gastrins extracted from hog antral mucosa". Gut 5: 103–14. doi:10.1136/gut.5.2.103. PMID 14159395. PMC: 1552180.|4. Lund T, Geurts van Kessel AH, Haun S, Dixon JE (1986). "The genes for human gastrin and cholecystokinin are located on different chromosomes". Hum. Genet. 73 (1): 77–80. doi:10.1007/BF00292669. PMID 3011648.|5. Vadokas B, Lüdtke FE, Lepsien G, Golenhofen K, Mandrek K (December 1997). "Effects of gastrin-releasing peptide (GRP) on the mechanical activity of the human ileocaecal region in vitro". Neurogastroenterol Motil. 9 (4): 265-270. PMID 9430795.|6. Valenzuela JE, Walsh JH, Isenberg JI (September 1976). "Effect of gastrin on pancreatic enzyme secretion and gallbladder emptying in man". Gastroenterology 71 (3): 409-411. PMID 950091.|7. Castell DO (February 1978). "Gastrin and lower esophageal sphincter tone". Arch. Intern. Med. 138 (2): 196. PMID 626547.
USBio References
No references available
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