Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pepsinogen is an inactive precursor of pepsin, a typical aspartic proteinases, synthesized in the chief cells of gastric glands. There are two major groups of pepsinogen, namely pepsinogen A (PGA) and pepsinogen C (PGC) (or progastricsin), and each frequently has isozymogens. The relative extents of expression of the two pepsinogens vary among animal species and, moreover, their biosynthesis is known to be affected by such bioactive peptides as gastrin and secretin; however, the regulation mechanism of pepsinogen biosynthesis, hence pepsinogen gene expression is not yet clear. Therefore, it is thought to be of fundamental importance to elucidate the primary structures of the pepsinogen gene for such studies. This report describes the primary structures of human PGA and PGC genes and rat PGC gene. The organization of the genes is essentially the same; each gene was found to be separated into nine exons by eight introns of various lengths, encoding the amino acid sequence of the corresponding prepepsinogen. These results show that these genes are all derived from a common ancestral gene. The 5'-flanking region of human PGA gene, however, was different from those of human and rat PGC genes, whereas those of human and rat PGC genes were similar to each other. Thus, it is suggested that the expression of the PGA and PGC genes are somewhat differently regulated.
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PMID:Gene structures of pepsinogens A and C. 145 84

In conscious, gastric fistula rabbits, gastric acid and pepsin secretion averaged 4.5 +/- 0.1 mmol/h (1.3 mmol.kg-1.h-1) and 4.9 +/- 0.3 IU/h (1.6 IU.kg-1.h-1), respectively; these values represent approximately 40-50% of maximal output. Basal serum gastrin concentrations averaged 24 +/- 4 pg/ml and did not correlate with basal acid secretion. Atropine and vagotomy incompletely inhibited basal acid secretion (by 84 and 50%, respectively) and completely inhibited 2-deoxy-D-glucose-stimulated gastric acid secretion. Atropine and vagotomy similarly inhibited basal pepsin secretion by 50 and 40%, respectively. Ranitidine decreased acid and pepsin secretion, but as with atropine, inhibition was not complete (73 and 37%, respectively). Although omeprazole did not affect pepsin secretion, omeprazole completely inhibited basal acid secretion and elevated postprandial intragastric pH above 5.0. Conscious, gastric fistula rabbits have the highest basal acid and pepsin output among species commonly studied. Both vagal-cholinergic pathways and histamine drive basal acid and pepsin secretion in the rabbit.
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PMID:Gastric acid and pepsin hypersecretion in conscious rabbits. 167 87

Spontaneous remission of gastric acid hypersecretion in the Zollinger-Ellison syndrome occurs rarely. This study shows the development of gastric secretory mucosal atrophy resulting in achlorhydria and loss of pepsin secretion in a 63-year-old woman with the Zollinger-Ellison syndrome. Reduced secretion began soon after starting treatment with omeprazole, and achlorhydria became complete 6 months later. The patient remains well with normal endoscopy results and is achlorhydric 4 years after the start of treatment and 34 months after stopping omeprazole. She was not colonized with Helicobacter pylori until 36 months after developing achlorhydria. Serum gastrin has increased from 1000 to between 5000 and 12,500 ng/L (pg/mL), was not suppressible by gastric acidification, and was not associated with G-cell hyperplasia. She also has a normal Schilling test and normal immunoglobulins, and lacks antibodies to parietal cells or H+, K(+)-ATPase. Moderate enterochromaffinlike cell hyperplasia is apparent for the first time on the latest biopsy sample.
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PMID:Development of sustained achlorhydria in a patient with the Zollinger-Ellison syndrome treated with omeprazole. 179 40

The acute effects of continuous intragastric administration of 1500 ml (4200 kJ/liter) of a polymeric and of a nonpolymeric formula on gastric function were studied in 15 healthy subjects. During 450 min 1500 ml, containing 6300 kJ (1500 kcal), was given through a nasogastric tube. At regular intervals the volume, the pH, the titratable acidity, and the pepsin activity of the gastric contents and the plasma gastrin concentration were determined. Maximal observed intragastric volumes occurred after 120 min (118 +/- 16 ml during polymeric formula, 212 +/- 37 ml during nonpolymeric one) and volumes subsequently halved (at 450 min 68 +/- 13 and 104 +/- 16 ml, respectively). During the administration of both polymeric and the nonpolymeric formula intragastric pH fell progressively to 3.15 and 2.67, respectively, at 450 min. Incremental plasma gastrin values increased between 120 and 450 min from 7 to 12 ng/liter during the polymeric formula. During the nonpolymeric one it stabilized after 120 min at 12 ng/liter. When the whole test periods were considered integrated, mean intragastric volumes tended to be larger during the nonpolymeric formula (153 +/- 23 ml) than during the polymeric formula (107 +/- 12 ml), but this difference was not statistically significant. Median integrated mean pH was lower during the nonpolymeric formula (2.89) compared with the polymeric one (3.26). Despite the limitation that the investigations were performed in healthy subjects only, it is concluded from this study that the risk of aspiration during continuous nasogastric tube feeding is probably greatest during the first few hours of administration because of the larger intragastric volumes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute effects of continuous nasogastric tube feeding on gastric function: comparison of a polymeric and a nonpolymeric formula. 190 Nov 12

We investigated the possible roles of centrally administered neuropeptide Y (NPY) on gastric secretion, serum gastrin levels and gastric mucosal blood flow in anesthetized rats. Centrally administered NPY dose-dependently stimulated gastric acid and pepsin secretion. The stimulatory effect of intracerebroventricular administration of NPY was more potent than that of intracisternal administration. Centrally administered NPY also increased gastric secretion in the central noradrenaline depleted rats. In contrast, intravenously administered NPY had no influence on gastric secretion. These stimulatory effects were abolished by vagotomy or atropine pretreatment. The serum gastrin levels did not change after central NPY injection. Although intravenously administered NPY slightly increased gastric mucosal blood flow, centrally administered NPY slightly diminished gastric mucosal blood flow. These results indicate that centrally administered NPY markedly influences gastric functions in the rat.
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PMID:Centrally administered NPY stimulated gastric acid and pepsin secretion by a vagally mediated mechanism. 192 94

In four gastric-fistula dogs, selective antral vagotomy markedly reduced the vagal stimulation of gastrin release, thereby defining both the vagal pathway for stimulation of gastrin and the anatomic source of such gastrin release. Despite loss of gastrin response, vagal excitation by 100 mg/kg 2-deoxy-D-glucose (2-DG) produced the same acid and pepsin responses after antral vagotomy as before, but there was an approximately 40% diminished fundic response to pentagastrin, histamine, and synthetic human gastrin, as well as to endogenous gastrin released by graded doses of bombesin. Bethanechol did not reverse the defect, ruling out inadvertent fundic vagal denervation, nor did raising serum gastrin by bombesin alter the response to vagal stimulation by 2-DG. Fundic response to bethanechol was increased by approximately 60%, and the output of gastrin increased at least fivefold after antral vagotomy. Gastrin responses to food were diminished and those to sham feeding were eliminated. Separation of the denervated antral pouch had no additional effect on acid secretion. Vagal stimulation of gastric secretion thus occurs almost exclusively through direct cholinergic effects on the fundus with little or no contribution from antral gastrin. Vagal denervation sensitizes the antrum to cholinergic stimulation.
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PMID:Effects of antral vagotomy in dogs on gastrin and gastric secretion with various stimuli. 197 63

Acid and pepsin are the major aggressive factors believed to play a role in the pathogenesis of peptic ulcer disease. On the average, patients with duodenal ulcer disease have higher than normal basal, nocturnal, and pentagastrin-stimulated acid secretion. Food-stimulated acid secretion, however, is normal in duodenal ulcer patients. The reason for higher basal and nocturnal acid secretion is not known but may be secondary to higher than normal basal serum gastrin concentrations in duodenal ulcer patients. Average serum pepsinogen levels also are higher than normal in patients with duodenal ulcer disease, suggesting that luminal pepsin concentrations also are higher. Patients with gastric ulcers have either normal or lower than normal acid secretion. This suggests that factors other than acid and pepsin may play a role in causing gastric ulcers. Reflux of bile and pancreatic juice into the stomach of patients with gastric ulcers has been suggested as one of the aggressive factors playing a role in the development of gastric ulcers.
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PMID:Role of aggressive factors in the pathogenesis of peptic ulcer disease. 211 15

We report a case of multiple duodenal ulcers with gastric hypersecretion due to a nongastrin secretagogue produced by a malignant tumor of the pancreas in a 78-year-old man. The case resembled a Zollinger-Ellison syndrome (ZES) with high acid output (basal acid output 27, sham meal-stimulated 37, maximum acid output 47 mEq/h), but with fasting gastrin 43 pg/ml, nonresponsive to secretin. As in ZES, pepsin output was comparatively low, and secretion was inhibitable by atropine (50% inhibited by 1 microM). The tumor removed at surgery contained less than 1 ng gastrin per gram, but was many times more potent than pentagastrin in stimulating acid from a lumen-perfused rat stomach. The tumor also contained cholecystokinin (CCK-8 and CCK-33), motilin, insulin, and somatostatin, which were also present in adjacent normal pancreas; in addition, the tumor contained pancreatic polypeptide and pancreatic cancer-associated antigen. This case represents a rare syndrome due to an as yet undefined peptide secreted by a (frequently malignant) pancreatic endocrine tumor and masquerading as ZES. This is the first report of studies of pepsin secretion and of the effect of atropine, suggesting that the physiologic effects of the secretagogue resemble that of gastrin.
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PMID:A nongastrin malignant ampullary tumor causing gastric acid and pepsin hypersecretion. A case report. 223 2

In the present paper, effects of scopolia drugs (scopolamine, anisodine, anisodamine) on experimental gastric mucosal lesion models in rats were investigated. Scopolia drugs were found to be effective anti-ulcer agents in three experimental gastric ulcer models (i.e. cold-restraint stress induced ulcer, indomethacin induced ulcer and acetic acid induced chronic ulcer) in rats in a dose dependent manner. Biochemical analysis of gastric juice and blood showed that scopolia drugs could inhibit gastric acid secretion and pepsin activity, increase gastric barrier mucus and concentration of serum gastrin, suggesting that these actions may contribute to its anti-ulcer effect.
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PMID:[Effect of scopolia drugs on the gastric mucosal lesion in rats]. 223 28

The effects of intrahyopthalamic microinfusions of corticotropin-releasing factor (CRF) on gastric bicarbonate, acid, and pepsin content and on cold restraint-induced gastric lesion formation were tested in three experiments. Bilateral microinfusions of CRF into the hypothalamic ventromedial nucleus (0.86 nmol/rat) significantly increased both gastric bicarbonate concentration and total bicarbonate output. These effects were observed irrespective of whether rats were pretreated with the acid antisecretory drug omeprazole. In nonomeprazole-pretreated rats, CRF microinfusions also significantly reduced acid secretion and raised pH. The increase in bicarbonate content accounted for half of the observed decrease in acid output, suggesting that CRF microinfusions activated separable bicarbonate-stimulating and acid-inhibiting hypothalamic systems. In non-omeprazole-pretreated rats, CRF microinfusions significantly increased serum gastrin, whereas pepsin output was unchanged. Gastric mucosal damage produced by 4 h of cold restraint was significantly diminished by CRF microinfusion into the ventromedial hypothalamus. These data demonstrate that ventromedial hypothalamic microinfusions of CRF increase bicarbonate content, decrease gastric acid content, and confer protection against cold restraint-induced gastric mucosal damage. Hypothalamic CRF neuronal terminals and receptors may be involved in the central regulation of gastric bicarbonate secretion as well as acid secretion.
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PMID:Intrahypothalamic corticotropin-releasing factor elevates gastric bicarbonate and inhibits stress ulcers in rats. 230 76


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