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)

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

An alpha fetoprotein (AFP)-producing tumour occurring in the head of the pancreas of a 30-year-old woman is reported. Histological examination revealed a markedly solid proliferation of tumour cells with prominent nucleoli and occasional luminal structures, some of which contained mucinous material stained with mucicarmine and alcian blue. No squamoid corpuscles were recognized. Immunohistochemistry showed intense positivity for lipase trypsin, and AFP basically, and single cells were also positive for carcino-embryonic antigen, CA19-9, synaptophysin and neuron-specific enolase. Pancreatic hormone-positive cells were absent. Electron microscopical examination revealed numerous granules of variable sizes in the tumour cells, which were considered to be zymogen. The tumour is an acinar cell carcinoma with multi-directional differentiation including the ability to produce AFP. Among AFP-positive pancreatic tumours, acinar cell carcinoma and pancreatoblastoma seem to be the most frequent.
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PMID:Alpha fetoprotein-producing acinar cell carcinoma of the pancreas showing multiple lines of differentiation. 754 Dec 76

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

Plasma pancreatic enzymes and hormones were longitudinally observed after producing partial obstruction of the major pancreatic duct in dogs to study an initial state of chronic pancreatitis or pancreatolithiasis. Fasting plasma immunoreactive cationic trypsin was elevated during the first six months and then decreased in a subgroup with pancreatic calculi, marked fibrosis, or duct dilatation when compared with the corresponding opposite at the end of the 12-month period. Similar but less prominent changes were found in fasting plasma immunoreactive pancreatic polypeptide (IRPP). Plasma amylase, glucose, or immunoreactive insulin or glucagon (IRG) show no significant variation. Plasma IRG and IRPP responses to intravenous insulin were reduced in the subgroups with marked pancreatic changes towards the end of the 12-month period. These results suggest that plasma pancreatic enzymes and hormones remain elevated as long as pancreatic damage is mild and then start to decline as the damage progresses in chronic pancreatitis or pancreatolithiasis.
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PMID:Longitudinal changes of plasma pancreatic enzymes and hormones in experimental pancreatolithiasis in dogs. 769 7

Somatostatin is a 14 amino acid peptide that inhibits pancreatic exocrine and endocrine secretion. Its clinical application has been limited by its very short half life, necessitating continuous intravenous infusion. Octreotide is an 8 amino acid synthetic analogue of somatostatin that possesses similar pharmacological effects. It has a much longer duration of action, however, and can be given subcutaneously. Both the intravenous and subcutaneous routes of injection of octreotide are well tolerated. Peak serum concentrations occur within 30 minutes after subcutaneous administration and within four minutes of a three minute intravenous infusion. Serum concentration increases linearly with dose. Octreotide is distributed rapidly, mainly in the plasma, where it is 65% protein bound. The elimination half life is about 1.5 hours and about 32% of a subcutaneous dose is excreted in the urine as unchanged octreotide. Octreotide inhibits gastroenteropancreatic secretion, especially of insulin, glucagon, pancreatic polypeptide, gastric inhibitory polypeptide, and gastrin. It also inhibits both release of thyroid stimulating hormone and growth hormone secretion in response to exercise, insulin induced hypoglycaemia, and argenine stimulation. Octreotide reduces splanchnic blood flow in healthy volunteers and hepatic venous pressure in cirrhotic patients. It can accelerate or delay gastric emptying, prolong transit time at moderate to high doses, stimulate motility at low doses, and inhibit gall bladder emptying. Octreotide considerably inhibits pentagastrin stimulated gastric acid secretion and significantly diminishes exocrine pancreatic function (amylase, trypsin, lipase). Octreotide increases intestinal transit time and decreases endogenous fluid secretion in the jejunum and ileum, thus increasing the absorption of water and electrolytes. These pharmacological effects of the analogue point to its therapeutic role in a variety of endocrine and gastrointestinal disorders.
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PMID:Somatostatin and somatostatin analogues: pharmacokinetics and pharmacodynamic effects. 791 41

Mediation of postprandial pancreatic enzyme secretion has been ascribed mainly to cholecystokinin and to vagovagal reflexes. Recent studies suggest that these pathways are subject to feedback regulation. Diversion of pancreatic juice from the duodenum stimulates cholecystokinin release and pancreatic enzyme secretion, and intraduodenal administration of trypsin or chymotrypsin inhibits cholecystokinin release and pancreatic secretion. The increased plasma cholecystokinin levels following diversion of pancreatic juice seems to be mediated by "cholecystokinin-releasing factor", a trypsin-sensitive substance secreted by the proximal small intestine. This factor may mediate pancreatic enzyme secretion in response to protein intake. Dietary protein in the intestine competes for the trypsin that would otherwise inactivate the factor. The resulting increase of this factor in the intestinal lumen releases cholecystokinin and stimulates pancreatic enzyme secretion. Enteropancreatic reflex can also be activated by distension or administration of hyperosmolar solutions in the duodenum eliciting pancreatic enzyme secretion without raising plasma cholecystokinin levels. This effect is inhibited by atropine, suggesting that it is cholinergically mediated. Pancreatic response to duodenal volume or osmolality is not suppressed by trypsin, indicating that the reflex is not affected by intraluminal proteases. Our studies also show that secretion of pancreatic polypeptide is under cholinergic control, and this peptide acts by interfering with cholinergic transmission, making it an ideal candidate to modulate pancreatic secretion stimulated by the vagal cholinergic pathway. Similar observations are made with somatostatin and calcitonin-gene related peptide which also acts preferentially to inhibit pancreatic secretion by the vagal cholinergic pathway.
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PMID:Negative feedback control of exocrine pancreatic secretion: role of cholecystokinin and cholinergic pathway. 791 21

Small fluctuations in cholinergic input may be involved in the regulation of human interdigestive pancreatic secretion. To determine the effects of small changes in cholinergic tone on phase II interdigestive trypsin secretion, we gave cholinergic agonists or antagonists to 17 healthy fasting subjects who underwent gastrointestinal intubation. Duodenal trypsin outputs, gastroduodenal motility, and plasma levels of pancreatic polypeptide (PP) as a marker of cholinergic tone were measured during intravenous infusion of bethanechol (0, 5, or 40 micrograms.kg-1.h-1) or atropine (0, 4, or 16 micrograms.kg-1.h-1) given during phase II alone or in combination based on a 3 x 3 factorial design. Data were evaluated by a response surface analysis of the average log values for the test period (using the average of log values of the control period as a covariate). Bethanechol increased trypsin output (p < 0.05) and plasma concentrations of PP (p < 0.05) within the ranges of spontaneous fluctuations of trypsin output and PP during phase II, but did not disrupt the periodicity of pancreatic secretion or the characteristic cyclical pattern of interdigestive motility and induction of phase III activity. Atropine markedly decreased trypsin output (p < 0.05) and plasma concentrations of PP (p < 0.05) and abolished the cycling of interdigestive pancreatic secretion and motor activity. These data suggest the hypothesis that cholinergic pathways participate in the control of interdigestive pancreatic secretion during phase II, while enzyme secretion during phase III may be regulated by other mechanisms.
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PMID:Cholinergic regulation of phase II interdigestive pancreatic secretion in humans. 809 37

A double-blind, randomized, placebo-controlled crossover study was performed to assess the influence of one week of selective M1-muscarinic receptor blockade on pancreatic exocrine secretion in man. Ten healthy subjects received telenzepine (3 mg p.o.) and placebo each for 8 days, with a 6-day drug-free washout interval between treatment sequences. On Day 8 of each sequence, pancreatic secretion was stimulated for 2 h by infusion of submaximal secretin (0.2 U.kg/h) followed by maximal stimulation with secretin (1.0 U.kg/h) and ceruletide (120 ng.kg/h). Telenzepine had no significant effect on secretory parameters during submaximal stimulation with secretin. During maximal stimulation, total protein, secretory volume, and output of amylase, trypsin and bicarbonate were unexpectedly increased by telenzepine. These findings might be partially explained by removal of the inhibitory influence of pancreatic polypeptide, which was depressed by telenzepine. Acute studies have shown that M1-receptor antagonists inhibit exocrine secretion. Our results suggest that adaptation of physiological mechanisms governing the exocrine pancreas may occur after one week of receptor blockade by a therapeutic dosage of telenzepine, to the extent that M1-blockade no longer inhibits secretion.
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PMID:Exocrine pancreatic secretion in man following one week of M1-muscarinic receptor blockade. 821 57

Pancreatic function tests were performed in 11 adult cystic fibrosis (CF) patients with a fecal fat excretion of more than 10% during treatment with pancrease 2 capsules three times a day. These tests included urinary p-aminobenzoic acid (PABA) excretion, fasting serum trypsin and pancreatic polypeptide (PP), and glucose and insulin in fasting and postprandial serum. Subsequently, the patients entered a double-blind placebo-controlled crossover study to assess the effect of gastric acid inhibition by 20 mg omeprazole on fecal fat excretion. Adjunct therapy with omeprazole resulted in a reduction of fecal fat excretion in patients with residual pancreatic function. This improvement showed significant positive correlations with urinary PABA excretion and the increase in serum PP after the meal (P < 0.02 and P < 0.05), but not with the other parameters studied. Therefore, the addition of omeprazole to pancrease is most successful in CF patients with residual pancreatic function, determined by urinary PABA excretion or incremental PP.
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PMID:Improvement of fecal fat excretion after addition of omeprazole to pancrease in cystic fibrosis is related to residual exocrine function of the pancreas. 842 Jul 40

To gain further insight on the effects of alcohol on human pancreatic enzyme secretion, we tested the effects of a 12% (v/v) alcohol solution, wine, and a glucose solution added to a meal on trypsin output in duodenal aspirate of nonalcoholic volunteers and compared the results to those of chronic alcoholics. Plasma concentrations of gastrin, cholecystokinin, and pancreatic polypeptide were monitored pre- and postprandially. Similar blood alcohol concentrations were determined in nonalcoholics and alcoholics following wine and the alcohol solution. Nonstimulated trypsin output (basal) was higher in alcoholics but not significantly so when compared to nonalcoholics. However postprandial trypsin output, 2014 +/- 301 mg/5 hr was significantly greater in alcoholics (P < 0.05) compared to nonalcoholics 1271 +/- 118 mg/5 hr. Alcohol and wine when added to the meal significantly (P < 0.05) inhibited trypsin output in both groups. Basal and postprandial levels of gastrin and cholecystokinin were similar in nonalcoholics and alcoholics. Basal plasma pancreatic polypeptide levels were similar in both groups, but the postprandial increments in pancreatic polypeptide levels observed in nonalcoholics were not observed in alcoholics. We conclude that chronic alcoholics have increased postprandial pancreatic enzyme secretion, and that this secretion, as that of nonalcoholics, can be affected by alcohol or wine. The postprandial hypersecretion of enzymes in alcoholics is not related to increased plasma levels of cholecystokinin or gastrin. It is possible that the impaired release of pancreatic polypeptide may participate in the mechanism for increased pancreatic enzyme secretion in chronic alcoholics.
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PMID:Pancreatic secretion in chronic alcoholics. Effects of acute alcohol or wine on response to a meal. 842 Jul 43


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