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)

Effects of several non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin (ASA), indomethacin (IM), flurbiprofen (FP), ibuprofen (IP), phenylbutazone (PBZ) and flufenamic acid (FA) were studied on the gastric ulceration and gastric acid secretion induced by restraint and water-immersion stress (RWIS) or various secretagogues in rats. These drugs significantly increased ulcer formation. IM (1, 3 and 10 mg/kg, s.c.) reduced gastric mucosal prostaglandin (PG) content dose-dependently. There was an appreciable correlation between this decrease in the PG content of gastric tissue and associated ulceration. The gastric acid secretion induced by the peripheral secretagogues, methacholine, gastrin and histamine, was not significantly influenced by IM pretreatment. In contrast, the gastric acid secretion induced by the vagal mediated secretagogues, insulin, 2-deoxy-D-glucose (2-D-G) and RWIS, was markedly increased by IM pretreatment. These effects were not observed in vagotomized rats. By intracerebroventricular (i.c.v.) injection of IM, no influence was observed on the gastric acid secretion and ulcer formation induced by 2-D-G or RWIS. These results suggest that acidic NSAIDs potentiate the gastric acid output induced by stimulation of vagus nerve activity, and prostaglandins (PGs) may influence gastric acid output by regulating vagus nerve activity.
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PMID:Possible involvement of non-steroidal anti-inflammatory drugs in vagal-mediated gastric acid secretion in rats. 388 88

The effect of oral omeprazole on insulin induced gastric secretion was studied in 12 healthy subjects. Each subject participated in two secretory tests receiving an intravenous infusion of insulin (0.03 units/kg/h) and being randomly allocated to receive 30mg or 60mg omeprazole suspended in 100ml water containing 16 mmol NaHCO3 on the second study day. Peak plasma concentrations of omeprazole were achieved within 30 minutes of administration in all but one subject and plasma half life was 30 minutes. Mean peak stimulated acid output in the six subjects receiving 30mg omeprazole was reduced to 4.3 +/- S.E. 1.8 mmol/h from a control value of 16.8 +/- 2.2 mmol/h (p less than 0.05) and in six subjects receiving 60mg omeprazole, mean peak output fell to 3.4 +/- 2.1 mmol/h from a control value of 12.3 +/- 2.6 mmol/h (p less than 0.05). The two doses of omeprazole produced similar reduction in acid secretion (74% and 73% respectively) but neither dose affected pepsin secretion. Both doses of omeprazole were associated with a small statistically insignificant increase in the plasma gastrin response to insulin infusion.
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PMID:The effect of omeprazole on insulin induced gastric secretion in man. 389 79

A novel stimulant of gastric acid secretion was extracted and purified from the non-antral gastric mucosa of the canine stomach and some of its biological properties were examined. Tissue was boiled in water and extracted in 2% trifluoroacetic acid. The stimulatory activity was purified by a combination of reverse-phase high pressure liquid chromatography (HPLC) and gel filtration. Fractions were assayed for a stimulation of basal, pentagastrin- and histamine-stimulated gastric acid secretion in the anaesthetized rat. Stimulatory activity was eluted from reverse-phase HPLC columns with acetonitrile and its elution from Sephadex G-10 and G-50 columns suggested a molecular weight of 1,000 to 3,000. The highly purified extracts enhanced basal, pentagastrin- and histamine-stimulated acid secretion in the rat. A stimulatory fraction was purified which was devoid of immunoreactive gastrin and gastrin-releasing peptide and contained only small amounts of histamine. Its chromatographic properties differed from those of histamine and acetylcholine. On two occasions the stimulant was purified to homogeneity and found to contain amino acids. Insufficient pure material was obtained for full characterization. The stimulant has been tentatively called oxyntin.
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PMID:Partial purification of a novel stimulant of gastric acid secretion from canine non-antral mucosa. 395 15

Water and electrolyte flux in response to systemic administration of four different gastrointestinal hormones were studied in a human with a chronic Thiry-Vella ileal loop. Gastrin infusion with a pharmacological dose of 4 micrograms/kg-hr has no effect. Responses to glucagon were proportional to infused doses with directly increased absorption of water and electrolytes (except bicarbonate). However, when gastrin was infused simultaneously with glucagon, the enhanced absorption was inhibited. Secretin only transiently increased absorption of fluid and electrolytes. In contrast to its effects on jejunum, CCK increased both water and electrolyte absorption from the ileum.
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PMID:Water and electrolyte absorption from a human Thiry-Vella ileal loop. Responses to systemic administration of gastrin, glucagon, secretin, and cholecystokinin. 396 99

The degree of tyrosine-O-sulfation and the ratio between large (gastrin-34 and component I) and small (gastrin-17 and -14) molecular forms of gastrin were studied in extracts of human fetal (n = 14) and adult (n = 9) antrum, duodenum, jejunum and pancreas. Boiled water extracts were applied to gel- and ion-exchange chromatography before and after treatment with trypsin and arylsulfatase. The fractions were monitored with sequence-specific radioimmunoassays that distinguish sulfated from non-sulfated gastrins. In antrum and duodenum about half the gastrins were sulfated at all stages of development. In the fetal jejunum gastrin occurred in sulfated form only while in the adult 72% (range, 64-88%) of the jejunal gastrins were sulfated. The larger molecular forms of gastrin predominated in the fetal compared with the adult antrum. In duodenum and jejunum, however, the ratio between small and large forms was the same in fetus and adult. Gastrin was undetectable in both fetal and adult pancreas. The results show that the degree of sulfation of gastrin varies substantially in the different parts of the gut at different stages of development. The differences may have functional significance, since sulfation increases the pancreozyminic and cholecystokinetic potency of gastrin.
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PMID:Complete sulfation of jejunal gastrin in the human fetus. 400 48

The effects of cholecystokinin (CCK) and gastrin on proximal and distal colonic motility were investigated because of the possible role of these peptides in feeding-induced colonic motility. Experiments were performed using 22 chloralose-urethane anaesthetized cats in which the colon was acutely denervated. The volume changes of the proximal and distal colon were recorded with water-filled flaccid balloons. The venous effluxes from the proximal and distal colon were recorded separately using drop recorder units. CCK-8, I-200 pmol X min-I close i.a., and pentagastrin, I-200 pmol X min-I close i.a., evoked dose-dependent contractions of the colon without altering systemic arterial blood pressure and colonic blood flow. The CCK peptides -8, -33 and -39 produced contractions of similar magnitude in the proximal and distal colon. The stimulatory effect of CCK-8 and pentagastrin on colonic motility was blocked by tetrodotoxin (I microgram X kg-I i.a.) and hexamethonium (I0 mg X kg-I i.v.). Atropine (0.5 mg X kg-I i.v.) completely blocked the responses to CCK-8 and pentagastrin in the distal colon but only partially in the proximal colon. Additional administration of naloxone (I mg X kg-I i.a.) abolished the remaining contractile response to the peptides in the proximal colon. The present results support the idea that CCK and pentagastrin have a stimulatory effect on distal colonic motility mediated via preganglionic and postganglionic cholinergic pathways. The possible role of opioid peptides and cholinergic mechanisms in the proximal colon is discussed.
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PMID:Atropine and naloxone block the colonic contraction elicited by cholecystokinin and pentagastrin. 401 85

This was a study of the effects of gastrin on gastric mucosal cyclic-adenosine 3':5'-monophosphate (cAMP)-dependent protein kinase activity and DNA synthesis in rat stomach carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in order to clarify the mechanism of the enhanced effect of gastrin on the early stage of stomach carcinogenesis. Inbred Basel-Wistar rats received MNNG in drinking water (50 micrograms/ml for 32 weeks) and were treated with s.c. injections of pentagastrin (300 micrograms/kg twice daily for 4 weeks) beginning with the fourth and eighth weeks after the initiation of MNNG treatment. The incidence of gastric adenocarcinoma in fourth-week gastrin-treated rats and of gastric carcinoid in eighth-week gastrin-treated rats was higher than that in rats treated with MNNG alone. The former tumors developed in the antrum and most of the latter tumors in the fundus. In the early stage of carcinogenesis the labeling index [( 3H]thymidine-labeled nuclei/one gland) in both the antrum and fundus was the same in MNNG-plus-gastrin-treated groups and in the MNNG-only-treated group. With regard to the distribution of cAMP-dependent protein kinase isoenzyme in fourth-week gastrin-treated rats, the proportion of type I cAMP-dependent protein kinase significantly increased in the antrum during the eighth week after the initiation of MNNG treatment (P less than 0.01). The increased type I activity in the antrum of the gastrin-treated rats agreed with the high incidence of gastric adenocarcinoma in the antrum. Type I isoenzyme clearly increased in gastric adenocarcinoma. These results suggest that type I cAMP-dependent protein kinase can play an important role in the enhanced effect of gastrin on rat stomach carcinogenesis induced by MNNG.
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PMID:Effect of gastrin on gastric mucosal cyclic adenosine 3':5'-monophosphate-dependent protein kinase activity in rat stomach carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine. 402 63

A radioimmunoassay has been developed using antibodies to a synthetic analogue of the C-terminal hexapeptide sequence of the porcine gastrin precursor. Boiling water extracts of porcine antral mucosa contained immunoreactive material that diluted in parallel with standard peptide. Concentrations of immunoreactivity were 5.5 +/- 0.8 nmol X g-1 (mean +/- S.E.M.) in antral mucosa and were closely similar to those of C-terminal heptadecapeptide gastrin immunoreactivity (5.0 +/- 0.6 nmol X g-1). Approximately 30-fold lower concentrations were found in porcine duodenum. A similar distribution was found in ferret, but human, rat and chicken antrum did not contain significant quantities of immunoreactivity. Gel filtration of porcine antral extracts on Sephadex G-50 revealed a single peak of immunoreactivity eluting in a similar position to G17, but on anion-exchange chromatography two peaks of immunoreactive material were separated. These also differed in their retention time on reverse phase HPLC. Both peptides are probably derived by tryptic cleavage at the C-terminus of porcine preprogastrin. No evidence was found to suggest that there are significant quantities of unprocessed preprogastrin in hog antral mucosa. The precise chemical difference between the two immunoreactive peptides identified here remains to be established; together, however, they provide specific markers for progastrin synthesis.
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PMID:Identification by specific radioimmunoassay of two novel peptides derived from the C-terminus of porcine preprogastrin. 403 6

Motilin, pancreatic polypeptide and gastrin blood concentrations in response to drinking water have been studied in 40 patients with functional bowel disease and compared with results in two groups of healthy control subjects. Patients with slow transit constipation and idiopathic megacolon showed impaired motilin release. Pancreatic polypeptide release was reduced in patients with slow transit constipation, but increased in those with functional diarrhoea. Gastrin release was impaired in all groups complaining of chronic constipation. Circulating motilin, pancreatic polypeptide and gastrin concentrations appear to bear some relationship to intestinal transit time in patients with functional bowel disorders.
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PMID:Positive correlation between symptoms and circulating motilin, pancreatic polypeptide and gastrin concentrations in functional bowel disorders. 405 4

The effect of incorporating guar gum into predominantly single-component meals of carbohydrate, fat or protein on liquid gastric emptying and on the secretion of gastric inhibitory polypeptide (GIP), gastrin and motilin, was studied in healthy human volunteers. Volunteers were given either 80 ml Hycal (carbohydrate meal), 150 g cooked lean minced beef (protein meal) or 200 ml double cream (fat meal) either with or without 5 or 6 g guar gum. Liquid gastric emptying was monitored in the fat and protein meals by taking 1.5 g paracetamol, consumed in water, with the meals and monitoring its appearance in circulation. Postprandial insulin and GIP levels were both significantly reduced by addition of guar gum to the carbohydrate meal. Postprandial GIP secretion was also reduced by addition of guar gum to the protein meal, but protein-stimulated gastrin secretion was enhanced by guar gum. There was a significant negative correlation between peak circulating gastrin levels and the corresponding GIP levels. Postprandial GIP secretion and plasma motilin levels were unaffected by addition of guar gum to the fat meal. 5 and 10 g guar gum/l solutions in water possessed buffering capacities between pH 2.75 and 5.5. Guar gum at 5 g/l caused no detectable change in liquid gastric-emptying time. The observed augmentation of gastrin secretion by guar gum following a protein meal could be due either to the buffering capacity of guar gum or to the attenuation of GIP secretion. It is possible that the chronic use of guar gum could be associated with changes in gastric acid secretion.
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PMID:The effect of guar gum on carbohydrate-, fat- and protein-stimulated gut hormone secretion: modification of postprandial gastric inhibitory polypeptide and gastrin responses. 406 84


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