Gastrin

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Gastrin
Identifiers
Symbol(s)	GAST; GAS
External IDs	OMIM: 137250 MGI: 104768 Homologene: 628
Gene ontology Molecular Function: • hormone activity Cellular Component: • extracellular region • soluble fraction Biological Process: • smooth muscle contraction • signal transduction
RNA expression pattern
More reference expression data
Orthologs
	Human	Mouse
Entrez	2520	14459
Ensembl	ENSG00000184502	ENSMUSG00000017165
Uniprot	P01350	Q6GSF5
Refseq	NM_000805 (mRNA) NP_000796 (protein)	NM_010257 (mRNA) NP_034387 (protein)
Location	Chr 17: 37.12 - 37.13 Mb	Chr 11: 100.15 - 100.15 Mb
Pubmed search	[1]	[2]

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In humans, gastrin is a hormone that stimulates secretion of gastric acid by the parietal cells of the stomach. It is released by G cells in the stomach and duodenum. 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]

Physiology

Genetics

The GAS gene is located on the long arm of the seventeenth chromosome (17q21).^[4]

Synthesis

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")
• gastrin-14 ("minigastrin")

The numbers refer to the amino acid count.

Release

Gastrin is released in response to certain stimuli. These include:

• stomach distension
• vagal stimulation (mediated by the neurocrine bombesin, or GRP in the human)
• the presence of partially digested proteins especially amino acids
• hypercalcemia

Gastrin release is inhibited by:

• The presence of acid (primarily the secreted HCl) in the stomach (a case of negative feedback).
• Somatostatin also inhibits the release of gastrin, along with secretin, GIP, VIP, glucagon and calcitonin.

Function

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 ECL cells.

Direct binding of gastrin to the parietal cells is involved in parietal cell maturation and fundul growth.

Gastrin also causes chief cells to secrete pepsinogen, the zymogen (inactive) form of the digestive enzyme pepsin. Pepsinogen is converted to pepsin in a low pH environment, and the HCl provides a suitable environment for its activity. It can also increase antral muscle mobility and trophic effect on GI tract and causes promotion of contraction of circular muscle of the stomach.

Gastrin has also been shown to induce production of pancreatic enzymes by acinar cells.

It increases gastric blood flow.

Factors influencing secretion

Gastric lumen:

• Stimulatory factors: dietary protein and amino acids, hypercalcemia. (i.e. during the gastric phase)
• Inhibitory factor: acidity (pH below 3) - a negative feedback mechanism, exerted via the release of somatostatin from δ cells in the stomach, which inhibits gastrin and histamine release.

Paracrine:

• Stimulatory factor: bombesin
• Inhibitory factor: somatostatin - acts on somatostatin-2 receptors on G cells. in a paracrine manner via local diffusion in the intercellular spaces, but also systemically through its release into the local mucosal blood circulation; it inhibits acid secretion by acting on parietal cells.

Nervous:

• Stimulatory factors: Beta-adrenergic agents, cholinergic agents, gastrin-releasing peptide (GRP)

Circulation:

• Stimulatory factor: epinephrine
• Inhibitory factors:gastric inhibitory peptide (GIP), secretin, somatostatin, glucagon, calcitonin

Role in disease

In the Zollinger-Ellison syndrome, gastrin is produced at excessive levels, often by a gastrinoma (gastrin-producing tumor, mostly benign) of the pyloric antrum 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.

References

1. ↑ Edkins JS (1906). "The chemical mechanism of gastric secretion". J. Physiol. (Lond.) 34 (1-2): 133–44. PMID 16992839. Full text at 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. PMID 8995084.
3. ↑ Gregory RA, Tracy HJ (1964). "The constitution and properties of two gastrins extracted from hog antral mucosa". Gut 5: 103–14. PMID 14159395. Full text at 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. PMID 3011648.

External links

• Overview at colostate.edu
• Physiology at MCG 6/6ch4/s6ch4_14

v • d • e Endocrine system: hormones/endocrine glands (Peptide hormones, Steroid hormones)
Hypothalamic-pituitary	Hypothalamus: TRH, CRH , GnRH, GHRH, somatostatin, dopamine - Posterior pituitary: vasopressin, oxytocin - Anterior pituitary: α (FSH, LH, TSH), GH, prolactin, POMC (ACTH, MSH, endorphins, lipotropin)
Adrenal axis	Adrenal medulla: epinephrine, norepinephrine - Adrenal cortex: aldosterone, cortisol, DHEA
Thyroid axis	Thyroid: thyroid hormone (T3 and T4) - calcitonin - Parathyroid: PTH
Gonadal axis	Testis: testosterone, AMH, inhibin - Ovary: estradiol, progesterone, inhibin/activin, relaxin (pregnancy)
Other end. glands	Pancreas: glucagon, insulin, somatostatin - Pineal gland: melatonin
Non-end. glands	Placenta: hCG, HPL, estrogen, progesterone - Kidney: renin, EPO, calcitriol, prostaglandin - Heart atrium: ANP - Stomach: gastrin, ghrelin - Duodenum: CCK, GIP, secretin, motilin, VIP - Ileum: enteroglucagon - Adipose tissue: leptin, adiponectin, resistin - Thymus: Thymosin - Thymopoietin - Thymulin - Skeleton: Osteocalcin - Liver/other: Insulin-like growth factor (IGF-1, IGF-2)
Target-derived	NGF, BDNF, NT-3

v • d • e Digestive system, physiology: gastrointestinal physiology
Enteric nervous system	Meissner's plexus - Auerbach's plexus
Exocrine	Chief cells (Pepsinogen) - Parietal cells (Gastric acid, Intrinsic factor) - Goblet cells (Mucus)
Endocrine/paracrine	G cells (gastrin), D cells (somatostatin) - ECL cells (Histamine) - enterogastrone: I cells (CCK), K cells (GIP), S cells (secretin)
Border	Brunner's glands - Paneth cells - Enterocytes
Fluids	Saliva - Bile - Intestinal juice - Gastric juice - Pancreatic juice
Processes	Swallowing - Vomiting - Peristalsis (Interstitial cell of Cajal) - Migrating motor complex - Borborygmus - Gastrocolic reflex - Segmentation contractions - Defecation

v • d • e Hormones: gastrointestinal hormones
CCK - EGF - GIP - Gastrin releasing peptide - Gastrins - Proglucagon - Motilin - Peptide YY -Prokineticin - Secretin - VIP

v • d • e Peptides: neuropeptides
Hypothalamic	Somatostatin - CRH - GnRH - GHRH - Orexins - TRH - POMC (ACTH, MSH, Lipotropin)
Gastrointestinal hormones	Cholecystokinin - Gastric inhibitory polypeptide - Gastrin - Motilin - Secretin - Vasoactive intestinal peptide
Other hormones	Vasopressin - Calcitonin -
Other	Angiotensin - Bombesin/Neuromedin B - Calcitonin gene-related peptide - Carnosine - Delta sleep-inducing peptide - FMRFamide - Galanin - Gastrin releasing peptide - Kinins (Bradykinin, Tachykinins ) - Neuromedin (B, N, U) - Neuropeptide Y - Neurophysins - Neurotensin - Opioid peptide - Pancreatic polypeptide - Pituitary adenylate cyclase activating peptide

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Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .

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