Gastrin is principally in charge of promoting the growth of the gastric mucosa, the function of the stomach, and the secretion of hydrochloric acid (HCl). The gastric antrum and duodenal G cells contain it. When peptides, amino acids, gastric distention, and a raised stomach pH are consumed, the vagus nerve and gastrin-releasing peptide (GRP), which are stimulated, are largely released. On the other hand, somatostatin’s paracrine suppression and a fall in stomach pH cause a reduction in gastrin secretion.
Gastrin hormone is an endocrine hormone that is secreted into the bloodstream by specialized cells called neuroendocrine cells. G cells are the particular neuroendocrine cells in charge of secreting gastrin. These cells are typically found in the stomach’s antrum, the area of the stomach that connects directly to the duodenum or the first segment of the small intestine. Gastrin causes the stomach to release gastric acid after a meal is consumed (hydrochloric acid).
Pepsinogen, a protein-digesting enzyme, is converted by gastric acid into pepsin. This is an active form that enables the stomach to digest proteins consumed as food and absorb several vitamins, including vitamin B12. Gastric acid also serves as a disinfectant, killing the majority of bacteria and other germs that enter the stomach with food and reducing the risk of gastrointestinal infection.
Gastrin stimulates the acid production from gastric parietal cells and mucosal development in the stomach’s acid-secreting portion, which are its two main biological functions. The increase in acid output that happens during and after meals is controlled by circulating gastrin. Additionally, gastrin promotes the development of stomach mucosa. In the proliferative zone, which is situated between the surface cells and the stomach glands in the acid-secreting mucosa, exogenously supplied gastrin increases cell division.
In addition, as refeeding promotes gastrin production and a concomitant rise in mucosal DNA synthesis, the increased mucosal proliferation that happens with refeeding after a period of fasting may be mediated by gastrin. In fasting rats, food and gastrin boost gastric ornithine decarboxylase mRNA and speed up cell division. In preliminary immunoneutralization studies, the gastrin antibody reduced the activation of ornithine decarboxylase caused by meals. In order to facilitate digestion, gastrin also enhances gut muscular contractions and induces the formation of the stomach lining.
The colon, duodenum, and pancreas have all been found to be affected by trophic effects of gastrin, however persistent hypergastrinemia does not appear to result in the hyperplasia of these organs. Therefore, it can be said that gastrin facilitates gastric mucosal proliferation that happens in response to feeding and hypochlorhydria and works as a physiological stimulant of both gastric acid secretion and gastric mucosal development.
The stretching of the stomach walls during a meal, the presence of specific meals (especially proteins) inside the stomach cavity, and an elevation in the pH levels of the stomach are all additional factors that induce the production of gastrin (i.e. the stomach becoming less acidic). Somatostatin, a hormone secreted by the pancreas when the stomach empties after a meal and when the stomach’s pH levels fall, inhibits the creation and release of gastrin (when the pH of the stomach becomes too acidic).
An overproduction of gastrin can result from a gastrinoma, also known as Zollinger-Ellison syndrome, that develops in the pancreas or the small intestine (more specifically, in the duodenum, which is the upper portion). High quantities of gastrin travelling throughout the gut in gastrinomas encourage the release of acid, resulting in ulcers on the lining of the stomach and small intestine that may rupture. Due to damage to the small intestine’s lining brought on by high stomach acid levels, diarrhoea can also result.
It’s crucial to take multiple endocrine neoplasia type 1 into account when gastrinoma is diagnosed (MEN1). Atrophic gastritis (when the stomach lining is damaged, chronically inflamed, and unable to produce and release acid), pernicious anaemia (a blood disorder caused by inadequate vitamin B12), and antacid medication use are just a few examples of conditions where high levels of circulating gastrin can occur.
Normal production of gastrin declines as stomach and intestinal acid levels rise. Low gastric acid can reduce the stomach’s capacity to absorb nutrition and raise the risk of intestinal infection.
According to studies, gastrin promotes cell invasion, migration, apoptosis, and tubulogenesis.
Gastrin was found in gastric antrum extracts in 1905, and it was recognised in 1964 as a pair of heptadeca peptides.
The stomach produces far too much acid when gastrin levels are elevated. The result of the extra acid is peptic ulcers and occasionally diarrhoea.
1. What is the primary purpose of gastrin?
Ans: The primary functions of the peptide hormone gastrin are to promote gastric mucosal development, gastric motility, and hydrochloric acid (HCl) secretion into the stomach.
2. What causes gastrin to be secreted?
Ans: In reaction to specific stimuli, gastrin is released. Stomach antrum distension is one of them. Stimulating the vagus (mediated by the neurocrine bombesin, or GRP in humans).
3. What organ secretes gastrin?
Ans: Gastrin is secreted at the pyloric end of a mammal’s stomach, which is where the small intestine meets the stomach. As a polypeptide made up of 14, 17, and 34 amino acids, gastrin can be found in humans in three different forms.
Anti-acid drugs you use for reflux or heartburn and a condition called chronic atrophic gastritis are by far the two most frequent causes of excessive gastrin levels.
Acetylcholine (Ach), which is released from vagal fibres via muscarinic receptors, directly stimulates gastrin release during the cephalic and oropharyngeal phases of a meal.
Caffeine, corticosteroids, and the blood pressure medications deserpidine, reserpine, and rescinnamine are among the medications that can lower gastrin levels.
1. What is gastrin and what is its primary role in the human body?
Gastrin is a crucial peptide hormone primarily responsible for regulating digestion. Its main function is to stimulate the parietal cells in the stomach lining to secrete hydrochloric acid (HCl). This acid creates the highly acidic environment necessary for digesting food, particularly proteins, and for killing ingested pathogens.
2. Where is the gastrin hormone produced?
Gastrin is secreted by specialised endocrine cells called G-cells. These cells are most abundant in the pyloric antrum, which is the lower part of the stomach. Smaller amounts of gastrin are also produced by G-cells in the duodenum (the first part of the small intestine) and the pancreas.
3. What are the main stimuli that trigger the release of gastrin?
The release of gastrin is triggered by several factors related to the intake of food. The main stimuli include:
4. What is the importance of gastrin in the process of protein digestion?
Gastrin plays an indispensable role in initiating protein digestion. It stimulates the release of HCl, which in turn converts the inactive enzyme pepsinogen (secreted by chief cells) into its active form, pepsin. Pepsin is the primary enzyme in the stomach that begins the breakdown of large protein molecules into smaller peptides.
5. How does the body prevent the overproduction of stomach acid using gastrin?
The regulation of gastrin operates on a negative feedback loop. As gastrin stimulates HCl secretion, the acidity in the stomach increases (pH level drops). Once the stomach pH falls below 3.0, the high acidity directly inhibits the G-cells, suppressing further gastrin release. This self-regulating mechanism ensures that the stomach does not become excessively acidic.
6. What is the main difference in function between the hormones gastrin and secretin?
Gastrin and secretin have opposing yet complementary functions in digestion. Gastrin works in the stomach to increase acid secretion in response to food. In contrast, secretin is released from the duodenum when acidic chyme (partially digested food) enters from the stomach. Secretin then stimulates the pancreas to release bicarbonate-rich fluid to neutralise the acid, protecting the small intestine.
7. What would be the physiological consequences if a person's body could not produce gastrin?
A lack of gastrin would lead to a condition called achlorhydria, the absence of stomach acid. This would have several negative effects:
8. Besides acid secretion, does gastrin have any other important functions?
Yes, while its primary role is stimulating acid secretion, gastrin also has other important functions. It promotes the growth and maintenance of the stomach lining (a trophic effect), helping it to repair and renew itself. Additionally, it stimulates gastric motility, which refers to the contractions of the stomach muscles that mix food with digestive juices and propel it towards the small intestine.