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)

The effects of alcoholic beverages on pancreatic secretion, blood trypsin levels, the release of gastrin and cholecystokinin were studied and compared with those of an alcohol and a glucose solution. Studies were done on six healthy male volunteers. The trypsin level was measured in the duodenal aspirate, while blood trypsin and gastrin levels were measured by radioimmunoassay and the cholecystokinin level was measured by bioassay. Studies were done on 5 different days, and on each day, the effects of either a glucose solution; an alcohol solution; or wine, beer, and gin solutions infused into the stomach were compared. The glucose solution stimulated trypsin secretion (a threefold increase above the basal measure) and the release of cholecystokinin without changes in the blood trypsin level. Blood alcohol levels, after the alcohol solution and all alcoholic beverages, were similar, and subjects showed mild symptoms of intoxication. Pancreatic enzyme secretion and trypsin blood levels were not significantly affected by either alcohol or the alcoholic beverages. Wine and beer caused significant release of gastrin and cholecystokinin. Under the conditions of this study, which reproduce those of excessive alcohol drinking, alcohol and alcoholic beverages did not stimulate pancreatic enzyme secretion, although wine and beer increased the release of gastrin and cholecystokinin. We conclude that alcohol and alcoholic beverages do not affect nonstimulated pancreatic enzyme secretion.
Pancreas 1989
PMID:Effect of alcohol and alcoholic beverages on nonstimulated pancreatic secretion in humans. 276 76

The effect of L-364,718, a cholecystokinin (CCK) receptor antagonist, on exocrine pancreatic secretion, gastric secretion, and plasma levels of gastrointestinal (GI) peptides stimulated by gastrin-releasing peptide (GRP) was examined in five conscious dogs. Intravenous infusion of graded doses of synthetic porcine GRP (18, 36, and 178 pmol/kg/h) caused significant and dose-dependent increases in pancreatic and gastric juice secretion and in plasma levels of pancreatic polypeptide (PP), CCK, and gastrin. Intravenous injection of L-364,718 (20 nmol/kg) significantly inhibited GRP-stimulated pancreatic outputs of juice volume, protein, and amylase and plasma PP release. L-364,718, however, did not affect gastric juice volume and plasma levels of CCK and gastrin. The results suggest that endogenously released CCK is, at least in part, responsible for GRP-stimulated pancreatic protein and enzyme secretions and PP release in dogs. The results further suggest that GRP-stimulated pancreatic secretion might be, in part, a direct response of GRP to exocrine pancreas.
Pancreas 1989
PMID:Effect of L-364,718 on GRP-stimulated pancreatic and gastric secretions and GI peptides in conscious dogs. 281 26

Bombesin, a 14-amino acid peptide, exhibits direct and indirect effects on the gastrointestinal tract, including release of hormones, stimulation of pancreatic, gastric, and intestinal secretion and intestinal motility. Cholecystokinin (CCK) and gastrin, two of the hormones released by bombesin, have been shown to play a role in maintaining the growth of normal gastrointestinal mucosa as well as in eliciting trophic responses in normal and neoplastic tissue. We studied the effects of chronic bombesin treatment on the growth of a human ductal pancreatic adenocarcinoma (SKI) xenografted into nude mice, and on the growth of the normal nude mouse pancreas. Thirteen nude mice were implanted with SKI tumor and divided into two groups. Mice received 0.1 ml intraperitoneal injections of either bombesin (20 micrograms/kg) or the vehicle alone three times per day. Tumor areas were measured twice weekly until death (week 8), at which time the tumors and the host pancreas were excised, weighed, and assayed for protein, RNA, and DNA content. Significant inhibition of tumor growth was found in the bombesin-treated group at weeks 4, 5, 6, 7, and 8. Tumor area and weight at death (day 57) were significantly less in the bombesin-treated group (48 and 46%) as compared with control. We observed similar inhibition of tumor DNA (39%), RNA (38%), and protein (43%) content compared with controls. In contrast, bombesin significantly increased the weight (64%), protein (81%), and DNA (73%) content of the mouse pancreas compared with controls. We conclude that bombesin acts concurrently as both a trophic agent for normal host pancreas and a growth inhibitory agent in xenografted pancreatic cancer tissue.
Pancreas 1988
PMID:Bombesin inhibits growth of human pancreatic adenocarcinoma in nude mice. 283 42

Surgical fragments of healthy and tumor-bearing pancreas from a patient with pancreatic tumor were studied by electron or light microscopy, histochemistry, and immunocytochemistry (human insulin, glucagon, somatostatin, gastrin, and bovine pancreatic polypeptide). Histological results were compared to those obtained by radioimmunoassay, both in tumor and serum. The tumor was identified as a glucagonoma because reactions for Grimelius' silver impregnation and immunoreaction with an antiserum against glucagon were positive and because a very high level of glucagon in the tumor was observed. Insulin, somatostatin, and gastrin levels remained normal, both in tumor and serum, but the glucagon level was normal in serum. Associated with this silent glucagonoma, an uncommon nesidioblastosis was also diagnosed with many A cells irregularly mixed with acinar cells, isolated or clustered in small groups. Acinar "intermediate" cells of "A" type were also observed. Such associative histopathological processes evoked possible development of an endocrine tumor from nesidioblastic-like tissue. Its embryogenic origin remained uncertain.
Pancreas 1988
PMID:Silent human pancreatic glucagonoma and "A" nesidioblastosis. 285 84

The effect of chronic administration of bethanechol and pentagastrin on the pancreas was examined. Rats were either antrectomized or subjected to a sham operation. Three weeks after surgery, rats received a daily intraperitoneal injection of either bethanechol (12 mg/kg) or pentagastrin (250 micrograms/kg) for 14 days. The fasting serum gastrin after bethanechol treatment increased to 1.89 times that of controls treated with saline. Although antrectomy decreased fasting serum gastrin to approximately 40% of controls, serum gastrin increased by 2.17 times that of the antrectomized rats and 1.37 times that of controls in the bethanechol group. After 14 days of bethanechol treatment, weight and amylase in the pancreas increased significantly compared with control; DNA and protein also increased 1.3 and 1.5 times that of control. The increase in DNA and pancreatic weight indicated that hyperplasia was the predominant mechanism. The pancreas showed atrophy in antrectomized rats but this was reversed by both bethanechol and pentagastrin. The results indicate that either endogenous gastric or extragastric gastrin release by cholinergic stimuli may have an important role in the regulation of pancreatic growth.
Pancreas 1986
PMID:Effects of bethanechol on the pancreas in antrectomized and normal rats. 288 4

Five patients with Zollinger-Ellison syndrome (ZES) have been treated during 9-12 months with long-acting somatostatin (SMS 201-995). Basal acid output presented a sustained decrease in 4 of 5 cases, below 10 mmol/h in three patients, allowing ranitidine discontinuation. No escape phenomenon was observed. Maximal acid secretion progressively decreased, suggesting an SMS antitrophic effect. Serum gastrin level was affected in a greater extent, showing a mean 87% decrease throughout the treatment period. Thus three patients kept normal serum gastrin levels in the long-term; one escaped to SMS after 9 months. Associated endocrine neoplasia were poorly influenced by SMS. No convincing evidence of tumor size variation was noted. Tolerance of SMS was excellent in the five patients. SMS' antitrophic and antigastrin properties could be of great interest in long-term management of ZES.
Pancreas 1988
PMID:Long-acting somatostatin (SMS 201-995) in the management of Zollinger-Ellison syndrome: evidence for sustained efficacy. 289 87

The effects of specific gastrin-cholecystokinin (CCK) receptor blockers (proglumide and a new, more potent product of Rotta Research Laboratorium, CR-1392) on pancreatic secretion were studied. Proglumide and CR-1392 caused a rightward and parallel shift, respectively, in the dose-response curve of CCK8 stimulated pancreatic protein secretion in anesthetized rats, demonstrating a competitive-like mechanism of inhibition. The mean PA2 values, demonstrating the 50% inhibitory dose of proglumide and CR-1392 were 3.7 and 5.7, respectively; i.e., CR-1392 proved to be about 100 times more potent than proglumide. In conscious rats, protein output and the volume of pancreatic juice were significantly decreased for about 2 h in response to 150 mg/kg of proglumide or 3 mg/kg of CR-1392 administered s.c. during diversion of pancreatic juice, demonstrating inhibition of endogenous CCK by glutaramic acid derivatives. Indeed, during reintroduction of precollected pancreatic juice into the duodenum, when the release of CCK is known to be almost totally eliminated, pancreatic secretion was not significantly modified by the same doses.
Pancreas 1988
PMID:The anti-CCK effect of glutaramic acid derivatives in anesthetized and conscious rats. 317 9

To determine the role of endogenous pancreatic polypeptide (PP) as a physiological inhibitor of pancreatic secretion, normal rabbit serum (control) or rabbit PP-antiserum was administered intravenously to dogs with chronic esophageal, gastric, and pancreatic fistulas. In all dogs tested, sham-feeding and ordinary feed with a meat meal resulted in a marked rise in the plasma level of immunoreactive PP that coincided with an increase in the exocrine pancreatic secretion of HCO3- and protein. After intravenous administration of PP antiserum, endogenous plasma PP was almost completely bound by infused antibodies to PP, whereas no such binding was detected after infusion of normal rabbit serum. In contrast, plasma gastrin remained unchanged both under basal and stimulated conditions. Immunoneutralization of PP, released endogenously, failed significantly to affect gastric acid and pancreatic protein responses to sham-feeding and the pancreatic HCO3- and protein responses to feeding a meat meal in chronic pancreatic fistula dogs. However, the PP antiserum abolished, in part, the inhibitory effect of exogenous PP on pancreatic secretion stimulated by exogenous hormones. We conclude that endogenous PP is not a physiological inhibitor of exocrine pancreatic secretion, as has been suggested previously.
Pancreas 1987
PMID:Immunoneutralization of circulating pancreatic polypeptide and pancreatic secretion. 331 80

To investigate the influence of beer on gastric and pancreatic secretion, 14 fasted volunteers were studied on two different days. A multilumen intestinal tube allowed measurement of intraluminal pressures and collection of gastric and duodenal juices. Seven subjects received in random order 250 ml of either beer or glucose (5.6%, w/v) intragastrically; seven other subjects received these intrajejunally. After 15 min, 48 +/- 8% of beer and 47 +/- 6% of glucose were emptied into the duodenum. Intragastric beer induced a nearly sevenfold increase in gastric acid output as compared with glucose (16.3 +/- 2.9 mmol/h versus 2.5 +/- 0.6 mmol/h; p less than 0.05), intrajejunal beer induced a nearly threefold increase (5.1 +/- 0.8 mmol/h versus 1.7 +/- 0.3 mmol/h). The stimulated gastric acid output was threefold higher after intragastric than after intrajejunal beer. Trypsin output was slightly but significantly (p less than 0.05) stimulated by intragastric beer as compared with glucose (4,639 +/- 460 U/h versus 3,628 +/- 399 U/h) and nearly threefold by intrajejunal beer (2,579 +/- 455 U/h versus 849 +/- 181 U/h) (p less than 0.05). Trypsin response to intragastric beer was 1.8 times higher than after intrajejunal beer (p less than 0.05). Intragastric beer induced a nearly ninefold increase of the 1 h integrated plasma gastrin response as compared with glucose (998 +/- 347 pM min vs 115 +/- 70 pM min) (p less than 0.05). Intrajejunal beer and glucose did not release gastrin. We conclude that both intragastric and intrajejunal beer stimulate gastric acid and pancreatic enzyme secretion; intragastric beer being a more potent stimulant. Gastrin might partially mediate the responses to intragastric but not to intrajejunal beer.
Pancreas 1988
PMID:Pancreatic and gastric responses to gastric versus jejunal beer in humans. 336 46

The effects of coffee on exocrine pancreatic secretion are unknown but may be important, because a link between chronic stimulation of pancreatic secretion and experimental chemical carcinogenesis and an association between coffee drinking and human pancreatic adenocarcinoma have been reported. We measured exocrine pancreatic trypsin and gastric acid secretions collected through orogastroduodenal tubes and serum gastrin in eight non-coffee drinkers and eight coffee drinkers. During fasting, after one interdigestive cycle control period, one of four 250-ml samples [plain water, water plus caffeine (4.6 mg/kg), decaffeinated coffee (127.9 mg/kg), caffeinated coffee (127.9 mg/kg)] was administered through the orogastric tube. Caffeinated and decaffeinated coffee (p = 0.008), caffeine (p = 0.03), and an unidentified substance(s) in coffee other than caffeine (p = 0.008) were associated with increased interdigestive exocrine pancreatic trypsin secretion. In addition, we also confirmed that coffee and caffeine stimulated gastric acid secretion (p = 0.02) and decaffeinated coffee raised serum gastrin concentrations (p = 0.005). If an association between coffee and pancreatic carcinogenesis exists, chronic stimulation of the exocrine pancreas by secretagogues could result in a gland susceptible to carcinogenesis.
Pancreas 1986
PMID:The acute effects of coffee and caffeine on human interdigestive exocrine pancreatic secretion. 357


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