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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, and gastrins were isolated in 1964 by Gregory and Tracy in Liverpool.
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Gastrin is released in response to certain stimuli. These include:
Gastrin release is inhibited by:
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
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 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 hypochlorhydia (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.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Gastrin". A list of authors is available in Wikipedia.|