Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of diverting bile from the duodenum in four dogs by cholecysto-jejunostomy was studied using a double-marker perfusion technique. During digestion of a liquid meal, acid secretion increased from 0.8 mmol H+/min to 1.48 mmol H+/min (p less than 0.05, paired t test); there was an associated rise in serum levels of gastrin 120 minutes after feeding (p less than 0.001, paired t test). Pancreatic secretion of trypsin decreased from 3.91 IU/min to 2.66 IU/min after bile diversion (p less than 0.01, paired t test) and the level of CCK was significantly lower 60 mins after feeding (p less than 0.05, paired t test). There was no significant change in the rate at which the liquid meal emptied from the stomach after bile diversion but the pH of duodenal contents was lower during the later stages of digestion. These changes may explain the reported increase of peptic ulcer after diverting bile from the duodenum and the procedure should not be considered unless the consequences of acid hypersecretion and pancreatic inhibition have been anticipated.
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PMID:Bile diversion from the duodenum: its effect on gastric and pancreatic function. 623 50

The cephalic phase of pancreatic secretion in humans was investigated using modified sham feeding and a duodenal perfusion system. Studies performed in 5 normal volunteers were designed so that trypsin and bicarbonate outputs during sham feeding, with or without pretreatment with atropine, were compared to "maximal" pancreatic secretory response to exogenous stimulation with caerulein and secretin. The role of gastric acid entry to the duodenum in mediating cephalic responses was assessed by a comparison between outputs observed when gastric aspiration (congruent to 80% efficient) was used alone and when acid entry was completely abolished by combining gastric aspiration with cimetidine pretreatment. To evaluate the role, if any, of gut hormone release in the pancreatic secretory response to sham feeding, plasma gastrin and cholecystokinin concentrations were monitored throughout. Trypsin outputs during sham feeding were 31.9 +/- 10.45 kallikrein inactivator units per 30 min, equivalent to four times basal output and 92% of maximal, but were only 54% maximal in subjects pretreated with cimetidine. Atropine suppressed basal trypsin output and abolished the response to sham feeding (4.98 +/- 3.89 kallikrein inactivator units per 30 min). A modest increase in bicarbonate secretion during sham feeding (3.30 +/- 1.97 mmol/30 min versus basal of 0.68 +/- 0.74 mmol/30 min, p = 0.5) was not influenced by atropine but was abolished by cimetidine pretreatment. No significant changes in plasma gastrins were observed in these studies and plasma cholecystokinins remained undetectable throughout. We conclude that there is tonic vagal stimulation of trypsin secretion, and that sham feeding markedly increases trypsin output, which is augmented further by acid entry into the duodenum. There is no direct effect of cephalic stimulation on bicarbonate secretion or on gastrin or cholecystokinin release.
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PMID:Sham feeding and pancreatic secretion. Evidence for direct vagal stimulation of enzyme output. 672 52

Two possibilities of an inhibition of gastric acid secretion are compared in regard to effectiveness and side effects. Combined i.v. bolus injection of 0.3 mg/kg cimetidine caused almost complete inhibition of peptone-stimulated acid secretion in normal volunteers and duodenal ulcer patients-radomized and double blind investigated-to the same extent as high dose secretin (3 CU/kg/h i.v. infusion) in normal volunteers. Postprandial gastrin was unchanged by combined drug application, but was suppressed by secretin. Temporary blurred vision, dry mouth, and signifiant increase of serum prolactin were side effects of the drug combination, whereas secretin caused dose-dependent diarrhoea, increaded diuresis and elecvation of serum lipase, trypsin, and sodium. Inhibition of acid secretion by combination of the antimuscarinic drug pirenzepine with the H2-receptor blocking substances cimetidine was almost complete, i.e. more effective than the combination of classic anticholinergics with H2-blockers tested so far. Inhibition of acid secretion by secretin was dose-dependent; the dosage clinically applied so far (10 CU/kg s.c. and 0.5 CU/kg/h i.v.) had the smallest effect. In spite of first favourable results with secretin in bleeding mucosal lesions, the observed side effects cast doubt on its broad clinical applicability. A controlled clinical trial of the combination of cimetidine plus pirenzepine as prophylaxis of bleeding from mucosal lesions in risk patients seems to be indicated.
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PMID:[Effectiveness of cimetidine, pirenzepine and synthetic secretin on stimulated gastric acid secretion]. 689 78

1. A standard duodenal perfusion technique was used to study the effects of luminally perfused sodium taurocholate on basal and stimulated biliary and pancreatic secretion and gastrointestinal hormone release in man. 2. During duodenal perfusion with sodium taurocholate alone, both basal and caerulein/secretin-stimulated bilirubin secretion were suppressed. A successive perfusion with a mixture of the bile salt and essential amino acids in combination overcame the biliary suppression and biliary secretion rose above basal levels. A further increase in bilirubin secretion was not observed in a subsequent perfusion with essential amino acids alone in these studies. 3. No inhibitory effect on basal or caerulein/secretin-stimulated trypsin secretion was observed during the bile salt perfusion; basal trypsin secretion was in fact slightly increased during a prolonged (4 h) perfusion of the bile salt. 4. During bile salt perfusion, basal bicarbonate secretion remained unchanged but caerulein/secretin-stimulated bicarbonate secretion was slightly increased. 5. Plasma levels of pancreatic polypeptide, gastric inhibitory peptide and gastrin did not change significantly during duodenal perfusion with bile salt, but plasma levels of motilin were suppressed. 6. These results support the view that bile salts in the duodenum may regulate biliary and pancreatic secretion in man and affect plasma levels of motilin.
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PMID:Duodenal perfusion with sodium taurocholate inhibits biliary but not pancreatic secretion in man. 708 56

The gastric effects of synthetic secretin given in a depot preparation as subcutaneous injection or in different doses as intravenous infusion were studied in 10 healthy volunteers. Peptone-stimulated gastric acid secretion and serum gastrin were significantly suppressed with a clear dose-response inhibition of acid output. There was a significant correlation between percentage inhibition of acid secretion and plasma secretin concentrations which were greatly above those seen physiologically. Serum lipase and trypsin increased significantly. Most subjects lost fluid from diuresis and diarrhoea, so that serum sodium and total protein concentrations also increased significantly. These side effects cast doubt on the clinical value of prolonged infusions of pharmacological doses of synthetic secretion in critically ill patients.
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PMID:Gastric effects and side effects of synthetic secretin in man. 728 Feb 90

1. Rat intestinal smooth muscle was shown to contain endogenous inhibitory activity towards the neutral trypsin-like muscle proteinase described previously [Beynon & Kay (1978) Biochem. J. 173, 291--298]. 2. Comtamination of the muscle tissue by mucosal, blood and pancreatic inhibitors was shown to be unlikely. 3. The inhibitory activity was resolved into high- and low-molecular-weight components. 4. The low-molecular-weight component was purified to homogeneity. It has a molecular weight of approx. 9000 and was stable over the pH range 3--11. 5. It inhibited the muscle proteinase competitively (Ki congruent to t microM), but had no effect on any of the other proteinases tested. 6. Leupeptin also inhibited the muscle proteinase competitively (Ki congruent to 0.3 microM), whereas the low-molecular weight proteins gastrin, glucagon and insulin B-chain had very little effect. 7. A role for a weakly binding inhibitor in modulating the influence of the neutral proteinase on intracellular protein degradation is considered.
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PMID:A low-molecular-weight inhibitor of the neutral proteinase from rat intestinal smooth muscle. 739 24

The new CCK-B/gastrin receptor antagonist PD 136450 is of potential value in treating neurologic and psychiatric disorders. We investigated possible side effects on the rat pancreas using acute and chronic administration schedules. In chronic experiments, four groups of rats were given either PD 136450, the proton pump inhibitor BY 308 (in order to induce hypergastrinemia), a combination of both, or control solutions over 14 d. Pancreatic growth, DNA, and protein content were significantly increased in rats given PD 136450 irrespective of circulating gastrin levels. Furthermore, an anticoordinate shift in pancreatic enzyme content in favor of trypsin and chymotrypsin at the expense of amylase and lipase was observed. Plasma CCK levels remained unchanged in this group making a role of circulating hormone unlikely. In order to investigate a possible direct agonist effect of the CCK-B/gastrin receptor antagonist, we studied amylase release from isolated rat pancreatic acini in response to PD 136450 and sulfated CCK8 alone and in combination with the specific CCK-A receptor antagonist MK 329. Increasing concentrations of PD 136450 caused a monophasic dose-response curve in contrast to the well-known biphasic amylase release in response to CCK8. Addition of increasing doses of PD 136450 to a concentration of CCK causing maximal stimulation of amylase release (0.1 nM) further enhanced amylase release from pancreatic acini. The specific CCK-A receptor antagonist MK 329 dose-dependently inhibited CCK8- and PD 136450-induced amylase release. In conclusion, the new CCK-B/gastrin receptor antagonist PD 136450 exhibited profound agonist actions on the rat pancreas mediated via CCK-A receptors.
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PMID:A new CCK-B/gastrin receptor antagonist acts as an agonist on the rat pancreas. 752 49

While pancreatic metaplasia has been observed in gastric mucosa of patients with chronic gastritis, it has not been described in ectopic gastric mucosa. We have identified focal clusters of cells resembling pancreatic acinar cells (CPACs) in 11 of 350 biopsies of Barrett's mucosa from 120 patients with Barrett's esophagus enrolled in a clinical efficacy trial of omeprazole versus ranitidine for treatment of gastroesophageal reflux disease. Three additional cases from our surgical files were also studied. Immunoreactivity for trypsin and chymotrypsin was present in the CPACs of all 14 cases, while stains for alpha-amylase and lipase were each positive in 12 of 13. A few cells in the CPACs were also positive for chomogranins (12 of 13 cases), serotonin (seven of 13 cases), somatostatin (three of 12), gastrin (four of 11), and pancreatic polypeptide (two of 13). No staining was seen for insulin or glucagon. Ultrastructural studies performed in one case showed features of pancreatic exocrine and endocrine (PP-type) cells in cells within CPACs. These results collectively indicate that the CPACs are aggregates of true pancreatic acinar cells admixed with a few endocrine cells. This pancreatic parenchyma in Barrett's mucosa is most likely of metaplastic origin and could be derived from the transitional zone cells or from pluripotent stem cells in the esophageal mucosa or from metaplasia of mucus cells. While the development of pancreatic metaplasia in Barrett's esophagus appears to be unrelated to drug therapy, the clinical relevance of this distinctive histological finding needs further investigation.
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PMID:Pancreatic metaplasia in Barrett's esophagus. An immunohistochemical study. 757 75

We here ascertain whether tryptase (a serine endoprotease released by mast cells) and cathepsin D (CD, a lysosomal hydrolase that seems able to derange the extracellular matrix) play a part in peptic ulcer disease and whether they are linked to Helicobacter pylori (Hp) infection. We studied 13 controls, 25 patients with gastric ulcer, 47 with duodenal ulcer, and 11 with duodenitis. Tryptase and CD were measured in mucosal biopsies (body and antrum of the stomach and duodenum) using IRMA methods. Hp infection was histologically evaluated (Giemsa). Tryptase and CD levels were higher (25%) in patients with active peptic ulcer, whether gastric or duodenal. In Hp-positive patients the CD mucosal content was higher while tryptase mucosal levels were lower than in Hp-negative patients. Tryptase was correlated with gastrin content. CD seems to be mainly related to the phlogistic reaction of the mucosa to Hp infection; tryptase may reflect an indirect link between Hp infection, gastrin release, and the function of mast cells.
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PMID:Influence of Helicobacter pylori on tryptase and cathepsin D in peptic ulcer. 758 35

Characterization of bombesin binding sites in healthy human lung was performed through direct binding techniques. There was limited binding in the absence of trypsin and chymotrypsin inhibitors, suggesting important activities of both enzymes in human lung and/or increased sensitivity of the bombesin sites toward them. In human lung membranes, bombesin, gastrin releasing peptide (GRP) and GRP-preferring bombesin receptor antagonists displaced [125I-Tyr4]bombesin binding with high affinities (36-177 nM), whereas neuromedin B possessed a lower affinity of 2878 nM. [D-F5Phe6,D-Ala11]bombesin-(6-13)-methyl ester, the most active GRP-preferring bombesin antagonist as yet reported, had the highest affinity among all antagonists tested whereas neuromedin B had the lowest affinity. These data demonstrate that the bombesin binding sites in the human lung are of the GRP-preferring type.
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PMID:Gastrin releasing peptide-preferring bombesin binding sites in human lung. 788 24


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