Gastric pepsinogen

The proteases are secreted as inactive zymogens the active site of the enzyme is masked by a small region of its peptide chain, which is removed by hydrolysis of a specific peptide bond. Pepsinogen is activated to pepsin by gastric acid and by activated pepsin (autocatalysis). In the small intestine, trypsinogen, the precursor of trypsin, is activated by enteropeptidase, which is secreted by the duodenal epithelial cells trypsin can then activate chymotrypsinogen to chymotrypsin, proelas-tase to elastase, procarboxypeptidase to carboxypepti-dase, and proaminopeptidase to aminopeptidase. 

Alterations in other gastric secretions, such as pepsinogens and blood group substances also take place in chronic atrophic gastritis. The secretion of pepsinogen I has been used as an indicator of intestinal metaplasia and gastric cancer (21, 22). 

Gastrin G cells in pyloric region of the stomach Protein in stomach vagal stimulation Stimulates parietal cells (HC1) and chief cells (pepsinogen) in stomach enhances gastric motility... 

Gastrin is a hormone produced by gastric endocrine tissue — specifically, the G cells in the pyloric gland area. It is released into the blood and carried back to the stomach. The major function of gastrin is to enhance acid secretion by directly stimulating parietal cells (HC1) and chief cells (pepsinogen). Gastrin also stimulates the local release of histamine from enterochromaf-fin-like cells in the wall of the stomach. Histamine stimulates parietal cells to release HC1. 

The gastric phase is elicited by the presence of food in the stomach. Distension of the stomach wall, as well as the presence of protein, caffeine, and alcohol, enhances gastric secretion. This phase is mediated by the intrinsic nerves, the vagus nerve, and gastrin. Each of these mechanisms promotes secretion of HC1 and pepsinogen. 

Gastric juice is the product of several cell types. The parietal cells produce hydrochloric acid, chief cells release pepsinogen, and accessory cells form a mucin-containing mucus. 

The hydrochloric acid in gastric juice is important for digestion. It activates pepsinogen to form pepsin (see below) and creates an optimal pH level for it to take effect. It also denatures food proteins so that they are more easily attacked by proteinases, and it kills micro-organisms. 

Gastric acid secretion is inhibited in the presence of acid itself. A negative feedback occurs when the pH approaches 2.5 such that further secretion of gastrin is inhibited until the pH rises. Ingested carbohydrates and fat also inhibit acid secretion after they reach the intestines several hormonal mediators for this effect have been proposed. The secretion of pepsinogen appears to parallel the secretion of H+, while the patterns of secretion of mucus and bicarbonate have not been well characterized. 

Xie G et al Cholinergic agonist-induced pepsinogen secretion from murine gastric chief cells is mediated by Mi and M3 muscarinic receptors. Am J Physiol 2005 289 G521. 

The digestion of proteins begins in the stomach, which secretes gastric juice—a unique solution containing hydrochloric acid and the proenzyme, pepsinogen ... 

Pepsinogen secretion from gastric chief cells Cholinergic vasodilatation in cerebral vessels... 

In the diet, vitamin B12 is bound to proteins. Although some release of protein-bound vitamin B12 begins in the mouth, most of the release occurs in the stomach on exposure of food to gastric acid (HC1) and the proteolytic enzyme pepsin. For this reason, either hypo-chlorhydria (abnormally low concentration of HC1 in gastric fluid) or achlorhydria (the absence of HC1 in gastric fluid) may decrease the availability of dietary vitamin B12 for absorption by preventing the activation of pepsinogen to pepsin, the principal enzyme responsible for proteolysis in the stomach. Achlorhydric patients with adequate production of IF may have low normal or subnormal serum B12 concentrations because of failure to liberate B12 bound to food. 

The entry of protein into the stomach stimulates the release of a hormone, gastrin, which then causes the release of hydrochloric acid from the parietal cells, and pepsinogen from the chief cells (Fig. 15-5). Pepsinogen is another zymogen (they all start with pro- or end in -ogen) that is converted in the gastric juice to the active enzyme pepsin. 

Pepsinogen is secreted by chief cells in the gastric mucosa and is the precursor of the protease enzyme pepsin. 

Q4 Water, mucus, pepsinogen and gastric lipase, which digests milk fats, are produced by the stomach. In young animals, rennin is also present in gastric secretions. The volume of secretion produced each day is approximately 21. 

Qll Both alcohol and the caffeine content of coffee act directly on the gastric mucosa to stimulate acid and pepsinogen secretion, so reduction in their use should help the patient. Smoking can also worsen dyspepsia (indigestion) and heartburn, possibly via actions of nicotine on the stomach wall. 

The alkaline buffers in the stomach may extract some preformed materials from gastric mucosa, such as pepsinogen, which normally would not enter the gastric lumen. 

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