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: UNIPROT:P61278 (somatostatin)
22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We demonstrated previously that pancreatic secretion of individual enzymes is specifically regulated (1). In the present study, we investigated and defined contributing roles of cholinergic and cholecystokinin tones to the specific regulation of rat pancreatic secretion of digestive enzymes. Animals were provided with pancreatic, biliary, duodenal, and jugular vein cannulas allowing separate drainage of bile and pure pancreatic juice, as well as intravenous infusions of MK329 or atropine sulfate along with SMS 201-995 (SMS). Rats kept in restraint cages were divided into four groups. The first rat group was infused with 5 micrograms kg-1 h-1 SMS alone; the second group was infused with a mixture of SMS and MK329 (5 micrograms kg-1 h-1:0.5 mg kg-1 h-1); the third group received a mixture of SMS and atropine (5 micrograms kg-1 h-1); and rats in the fourth group were administrated a mixture of SMS, MK329, and atropine (5 micrograms kg-1 h-1:0.5 mg kg-1:100 micrograms kg-1 h-1). Food, but not water, was denied rats 10 h before the experiment and throughout the 6-h experimental period. During the experiment, pancreatic juice was continuously collected every 15 min from each rat, and a 15-microliter aliquot of the pancreatic juice sample was removed for total protein, amylase, lipase, trypsinogen, chymotrypsinogen, and proelastase assays. Pancreatic juice previously collected from a donor rat was mixed with the fresh bile and the mixture was recirculated into the duodenum. The secretory patterns over the 6-h experimental period showed that during the first hour of drug infusion, MK329 alone did not alter the SMS-induced inhibitory process of total protein and amylase, trypsinogen, and proelastase secretion, and there was no marked change in total protein and enzyme outputs. Adding atropine to SMS did not alter the secretory pattern during the first hour of drug infusion, but a significantly greater decrease in protein and enzymes outputs occurred. Correlations between paired enzyme outputs greatly increased with SMS alone, but some changed when either MK329 or atropine was infused along with SMS. When all drugs were infused together, enzyme outputs became strongly correlated. These results suggest that under fasting conditions, somatostatin and atropine can neutralize basal pancreatic enzyme outputs, leading to a constitutive type of secretion characterized by parallel secretion of the digestive enzymes. Furthermore, it is proposed that under basal secretion conditions, acetylcholine and cholecystokinin reaching the pancreatic acinar cells may act to dissociate pancreatic secretion of individual digestive enzymes originating from heterogeneous secretory granules.
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PMID:Modulation of pancreatic secretion of individual digestive enzymes in octreotide (SMS 201-995)-infused rats. 898 7

The aims of medical therapy in chronic pancreatitis are mainly to relieve the recurrent pain and to correct any malabsorption secondary to digestive insufficiency resulting from deficient exocrine pancreatic function. The treatment of the pain initially involves the use of dietary measures and analgesic drugs. The results of the use of pancreatic extracts and somatostatin reported in the literature are controversial, as are those of coeliac plexus block. Of unquestionable efficacy, at least in the short to medium term, are surgical decompression interventions in patients, with pain refractory to these measures and who present significant dilation of Wirsung's duct at ERCP. Endoscopic decompression constitutes an alternative to surgical decompression. In view of the transitory results of endoscopic decompression, which, in any event, should be implemented only by endoscopists possessing the necessary experience and expertise, the use of this technique may perhaps be targeted at carefully selected patients to be submitted to surgical decompression. As far as maldigestion is concerned, which occurs only when the pancreatic functional deficit reaches 90% or more, replacement therapy with pancreatic extracts must be resorted to. Multi-Unit Dose preparations are to be preferred, consisting in gastro-protected microspheres measuring not more than 2 mm in diameter and containing high doses of lipase, since at least 30,000 I.U. of lipase are required in the post-prandial phase for reasonably satisfactory correction of the steatorrhoea. Should this fail to prove effective, it is good policy to add antisecretory drugs (H2-antagonists, proton-pump inhibitors).
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PMID:[The medical therapy of chronic pancreatitis. Problems, progress and outlook]. 902 57

Bile salts are intraduodenal stimulants of basal pancreatic secretion. This study aims to show whether the three main bile salts of human bile differ in their action on pancreatic secretion, and whether they enhance or inhibit each other after combined use. Furthermore, the effect on gastroenteropancreatic peptide release is evaluated. Twelve subjects were provided with a gastroduodenal double-lumen tube. Equimolar doses (0.6 mmol) of taurocholate (322 mg), taurodeoxycholate (313 mg), and a combination of both stimuli were given intraduodenally. Another 12 subjects received taurochenodeoxycholate (313 mg) instead of taurocholate. Volume, bicarbonate, trypsin, and lipase were determined in duodenal aspirates. Cholecystokinin, pancreatic polypeptide, and somatostatin were measured radioimmunologically in plasma samples. All bile salts and combinations exerted a significant hydrokinetic and ecbolic effect. The hydrokinetic response of the combined stimuli was significantly higher as compared with taurocholate and taurochenodeoxycholate, respectively. As far as concerns the ecbolic response, the difference was significant only for trypsin output as compared with taurochenodeoxycholate. Plasma cholecystokinin rose significantly only after the combined stimuli. Pancreatic polypeptide and somatostatin increased significantly after all stimuli, except pancreatic polypeptide after taurocholate. Combined use enhances the hydrokinetic and ecbolic effects of single bile salts. Cholecystokinin may, hereby, be involved as a mediator of the ecbolic effect. Pancreatic polypeptide release indicates cholinergic mechanisms as further mediators. As demonstrated by somatostatin release, counter-regulatory mechanisms are also triggered by intraduodenal bile salts.
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PMID:Exocrine pancreatic secretion and plasma levels of cholecystokinin, pancreatic polypeptide, and somatostatin after single and combined intraduodenal application of different bile salts in man. 903 83

The authors investigated the effects of glucagon and a somatostatin preparation (Stilamin) on the secretion volume and on the secreted and absorbed enzyme levels of the pancreas. Four groups of dogs with an artificial pancreatic fistula were given a single intravenous injection of glucagon (group I, n = 8), intravenous drip-infusion of glucagon (group II, n = 8), intravenous drip-infusion of somatostatin (group III, n = 10) and intravenous drip-infusion of the carrier fluid, physiological sodium-chloride (control, group IV, n = 5), respectively. Pancreatic juices were collected and volume, pH, bicarbonate, amilase, lipase, trypsin and protein contents were determined. Serum amilase and lipase levels before and at the termination of the experiment were also measured. Intravenous drip-infusion of both Glucagon and Stilamin decreased pancreatic secretion, Stilamin being more effective than Glucagon. On the other hand, a single i.v. injection of Glucagon resulted in an increased secretion. The authors suggest that based on the observed inhibitory effect on pancreatic secretion, both glucagon and somatostatin could be used to reduce postoperative complications of pancreatic operations in the clinical practice.
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PMID:Effect of glucagon and somatostatin on pancreatic secretion in dogs. 904 60

Infection with Helicobacter pylori (H. pylori) is now recognized as a major factor in the pathogenesis of gastric disease, and the successful therapy regimens require a combination of H2 blockers with gastroprotective and antimicrobial agents. Ebrotidine (N-[(E)-[[2-[[[2-[(diaminomethylene) amino]-4-thiazolyl] methyl]thio]ethyl]amino]methylene]-4-bromo-benzenesulfonamide, CAS 100981-43-9, FI-3542) is the only drug combining acid-suppressant activity with remarkable gastroprotective and anti-H. pylori properties. The drug not only displays a potent anti-H. pylori activity alone, but also exerts a strong potentiating effect on the efficacy of antimicrobial agents commonly used for H. pylori eradication, and the successful ulcer therapy with ebrotidine induces a significant (4-fold) increase in the H. pylori aggregation titer of gastric mucin. Moreover, the drug exhibits a strong inhibitory effect on H. pylori urease activity, the extent of which exceeds that of ranitidine, omeprazole and lansoprazole. Ebrotidine has also been demonstrated to exert a potent inhibitory action on the enzymatic activities directed towards mucus perimeter of gastric mucosal defense, causing a marked inhibition of H. pylori protease, lipase and phospholipase A2 activities. Another important property of ebrotidine is its ability to efficiently counteract the disruptive effects of H. pylori lipopolysaccharide on the integrity of gastric epithelium. This includes countering the interference by the lipopolysaccharide in mucosal integrin receptor interaction with proteins of extracellular matrix and the reversal of H. pylori disruptive effect on the binding of mucin to its gastric epithelial receptor. Furthermore, most recent data indicate that ebrotidine has the ability to reverse the impairment caused by H. pylori in feedback inhibition of gastrin release by somatostatin. This activity of ebrotidine apparently stems from the drug's ability to counter the untoward effect of H. pylori on the binding of somatostatin to its specific receptor on the gastric mucosal G-cells. The unique combination of acid suppressant, gastroprotective and anti-H. pylori activities makes ebrotidine a drug of choice in the treatment of gastric disease caused by H. pylori.
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PMID:Anti-Helicobacter pylori activities of ebrotidine. A review of biochemical and animal experimental studies and data. 920 47

Although clusters of pancreatic acinar cells (CPACs) have been reported in gastric mucosa of adults, they have not been described in children. We reviewed 283 pediatric gastric (239 antral and 44 corpus) mucosal biopsies during a 2-year period and detected CPACs in 10 antral biopsy samples. These biopsy samples were stained immunohistochemically for pancreatic exocrine markers (trypsin, chymotrypsin, alpha-amylase, and lipase) and a panel of regulatory substances (insulin, glucagon, somatostatin, pancreatic polypeptide, gastrin, and serotonin). Double immunostaining for colocalization of chromogranins and trypsin as well as mucin and trypsin also were performed on all cases. CPACs were seen in antral mucosa in a background of either normal or minimally inflamed mucosa, without any atrophy or metaplasia, and were positive for all pancreatic exocrine markers. Stray chromogranin-positive cells in the CPACs were also immunopositive for somatostatin, gastrin, or serotonin. All CPACs showed a few hybrid (amphicrine) cells that coexpressed both chromogranin and trypsin. In one case, ultrastructural examination showed such cells to contain both zymogen and neurosecretory granules. Although the presence of CPACs exclusively in the antrum is most likely the result of a sampling bias, the presence of hybrid cells with an amphicrine phenotype suggests that CPACs probably result from an aberration of stem cell differentiation.
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PMID:Pancreatic acinar cell clusters in pediatric gastric mucosa. 942 22

Intraduodenally applied bile salts and essential amino acids are known to stimulate exocrine pancreatic secretion. There are contradictory reports, however, about an interaction of both stimuli with respect to pancreatic function. The intention of the study was to compare the effects of equimolar amounts of taurodeoxycholate and L-phenylalanine used singularly and combined on pancreatic secretion and on gastroenteropancreatic peptide release. In 12 healthy subjects, 0.8 mmol of Na-taurodeoxycholate (410 mg) and L-phenylalanine (130 mg) were separately and combined applied into the duodenum in a randomized order. Volume, bicarbonate, trypsin, lipase, and amylase secretion as well as cholecystokinin, pancreatic polypeptide, and somatostatin plasma levels were measured. Volume and bicarbonate secretion was significantly enhanced by taurodeoxycholate. The effect was stronger compared to L-phenylalanine. The increase of enzyme secretion was comparable. After combined application, the ecbolic effect was insignificantly smaller, whereas the hydrokinetic effect was between those of the single stimuli. Plasma levels of cholecystokinin, pancreatic polypeptide, and somatostatin rose concomitantly with the pancreatic response. On an equimolar basis taurodeoxycholate results in a stronger hydrokinetic effect than L-phenylalanine. Their ecbolic effects, however, are comparable. In addition to cholinergic mechanisms, as indicated by the PP release observed, cholecystokinin may also act as a mediator. In combined application, the stimuli interfere with each other. Somatostatin and pancreatic polypeptide are not responsible for this mutual inhibition.
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PMID:Effect of intraduodenal taurodeoxycholate and L-phenylalanine on pancreatic secretion and on gastroenteropancreatic peptide release in man. 943 49

Cyclo(PheN2-Tyr-D-Trp-Lys-Val-PheC3)-Thr-NH2 (PTR 3046), a backbone-cyclic somatostatin analogue, was synthesized by solid-phase methodology. The binding characteristics of PTR 3046 to the different somatostatin receptors, expressed in CHO cells, indicate high selectivity to the SSTR5 receptor. PTR 3046 is highly stable against enzymatic degradation as determined in vitro by incubation with rat renal homogenate and human serum. The biological activity of PTR 3046 in vivo was determined in rats. PTR 3046 inhibits bombesin- and caerulein-induced amylase and lipase release from the pancreas without inhibiting growth hormone or glucagon release. The major conformation of PTR 3046 in CD3OH, as determined by NMR, is defined by a type II' beta-turn at D-Trp-Lys and a cis amide bond at Val-PheC3.
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PMID:A backbone-cyclic, receptor 5-selective somatostatin analogue: synthesis, bioactivity, and nuclear magnetic resonance conformational analysis. 952 66

The effects of somatostatin and octreotide (a long acting somatostatin analogue) in acute pancreatitis are inconclusive. This study examined the prophylactic and therapeutic effects of different doses of octreotide on retrograde sodium taurodeoxycholate-induced acute necrotizing pancreatitis in rats. The rats were divided into 4 groups receiving subcutaneous injection of saline, octreotide 10 microg/kg, 20 microg/kg at 0, 8 and 16 h and octreotide 20 microg/kg at 5, 13 and 21 h, separately. The serum levels of amylase and lipase, pancreatic histopathology, mortality and hemodynamics were examined. Octreotide significantly reduced serum levels of amylase and lipase at 12 h and the degree of pancreatic edema, necrosis and hemorrhage at 18-24 h as compared to the control group. Prophylactic octreotide 10 microg/kg significantly decreased the 24-h mortality from 100% to 44.4% (p < 0.05). The 24-h mortality further reduced to 12.5% and 10% with prophylactic and therapeutic octreotide 20 microg/kg, respectively. The decrease of mean arterial pressure at 12 h was significantly lower in octreotide groups than in the control group. We conclude that octreotide improves pancreatic histopathology and survival in acute necrotizing pancreatitis in rats.
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PMID:Effects of high dose octreotide on retrograde bile salt-induced pancreatitis in rats. 953 43

This study was designed to examine the role of somatostatin in regulating changes in lipid metabolism of larvae and metamorphosing landlocked sea lamprey, Petromyzon marinus. Larvae and animals in late metamorphosis (stage 6 on a 7-stage scale) were injected intraperitoneally once per day for 2 days with either saline (0.6%) or somatostatin-14 (SS-14; 500 ng/g body wt). Injection of SS-14 into larval and stage 6 metamorphosing animals resulted in elevated plasma fatty acids levels. In larvae, SS-14-induced hyperlipidemia was supported by enhanced lipolysis, as indicated by increased triacylglycerol lipase (TGL) activity in the liver and kidney. Mobilization of larval renal lipid was accompanied by reduced TG synthesis, as indicated by decreased diacylglycerol acyltransferase (DGAT) activity. In stage 6 metamorphosing lamprey, SS-14 did not significantly affect TGL activity; however, SS-14 significantly reduced fatty acid synthesis, as measured by acetyl-CoA carboxylase activity, in kidney, liver, and muscle, as well as muscular TG synthesis. SS-14-stimulated lipid depletion is reminiscent of the pattern of lipid metabolism displayed by P. marinus during their spontaneous metamorphosis-an observation which suggests that somatostatin may play a role in metamorphosis-associated changes in lipid metabolism in this species.
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PMID:Effects of somatostatin on lipid metabolism of larvae and metamorphosing landlocked sea lamprey, Petromyzon marinus. 967 89


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