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)

With a view toward the therapeutic use of somatostatin in the treatment of acute pancreatitis, a preliminary investigation was conducted with 6 healthy volunteers, in which the suppressive effect of somatostatin on endocrine and exocrine pancreatic function was observed. A 30-minute baseline measurement period was followed by the administration of cyclic somatostatin (100 microgram by i.v. injection plus a 90-minute infusion at a rate of 200 microgram/hr). After the first 45 minutes of this infusion secretion was submaximally stimulated by the infusion of secretin-cholecystokinin-pancreozymin (CCK-PZ) (75 U each), over two hours. No decrease was observed in basal bicarbonate or enzyme concentration under somatostatin administration alone. However, secretion did not show the usual steep rise after the commencement of stimulation. After the somatostatin infusion was stopped, i.e. under secretin-CCK-PZ alone, a significant increase occurred in the values of secretin-induced volume, bicarbonate concentration and total bicarbonate contents of the duodenal aspirate, as well as in CCK-PZ-induced enzyme secretion. The release of insulin, both basal and stimulated, was also significantly decreased by somatostatin.
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PMID:[Suppressive effect of somatostatin on secretin-CCK-PZ-stimulated endocrine and exocrine pancreatic function in man (author's transl)]. 41 Jan 66

Somatostatin was prophylactically administered to 10 patients who had surgery for pancreatic diseases. The postoperative course uncomplicated with no increase in serum amylase levels. Bile induced acute pancreatitis in six beagles was prophylactically treated with somatostatin. The results demonstrate that SRIF not only inhibits basal but also pancreatic-induced blood amylase and enzyme activities in the dog. SRIF-treated animals were in good general condition compared with untreated controls, macroscopic and histologic aspects of the pancreas were significantly improved.
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PMID:[Prevention of postoperative pancreatic complications following duodenopancreatectomy using somatostatin]. 47 69

Because somatostatin (SRIF) reduces exocrine pancreatic secretion, its effect on acute pancreatitis was investigated in rats. Linear SRIF reduced serum amylase and lipase but had no effect on pancreatic necrosis, oedema, leucocyte infiltration, and enzyme content. The mortality rate was not reduced. These results do not recommend the use of SRIF in the treatment of acute pancreatitis.
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PMID:Somatostatin therapy of acute experimental pancreatitis. 60 91

To evaluate the action of somatostatin on exocrine and endocrine pancreatic function, synthetic somatostatin (GIF) was administered (intravenous bolus of 300 mug followed by a constant 60-minute infusion, 5 mug/min) to 17 normal subjects. The secretin-induced volume and total bicarbonate contents of the duodenal aspirate were not affected whereas the bicarbonate concentration was significantly diminished. GIF reduced decisively the pancreatic enzyme secretion stimulated by pure (99%) cholecystokinin-pancreozymin. After the GIF infusion was stopped, a significant rise in enzyme secretion was observed. The secretin-induced insulin release was almost completely suppressed. Because GIF can be extracted in large quantities from pancreas, these data suggest that somatostatin may play a physiological role in the regulation of the secretory processes of this organ. Furthermore, GIF may be a useful adjunct in the treatment of acute pancreatitis.
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PMID:Effects of somatostatin on exocrine and endocrine pancreatic function stimulated by intestinal hormones in man. 76 55

Glucagon is secreted not only by A2-cells of the pancreatic islets but also by A cells in the gastric fundus and duodenum. Several reports have demonstrated that the glucagon plasma concentration is increased in genetic diabetes as well as in many conditions associated with a decreased glucose tolerance such as hepatic cirrhosis, myocardial infarction, infectious diseases, burns, taumatic shock, glucagonomas, acute pancreatitis, acromegaly, pheochromacytoma and Cushing's syndrome. Hyperglucagonemia is particularly important in diabetic ketoacidosis and in non-ketotic hyperosmolar coma. The mechanisms responsible for the diabetic's hyperglucagonemia remain controversial. According to several authors, the increased glucagon secretion is, for its main part, secondary to a prolonged defect in insulin secretion and thus relatively insensitive to an acute insulin administration. According to others, the A cell abnormality is of primary origin, independant from insulin deficiency and its effects are cumulative with those of the insulin lack. Several reports dealing with induced or spontaneous experimental diabetes are in favor of the first or the second hypothesis. It appears likely that glucagon plays a role in the metabolic derangments of diabetes. Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. These results illustrate the contribution of glucagon in the pathogenesis of hyperglycemia and ketosis. Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Although controversial, the role of glucagon in ketogenesis appears likely.
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PMID:[The role of glucagon in hyperglycemia. A review (author's transl)]. 79 28

Although calcitonin and somatostatin are polypeptid hormones of entirely different structure, in pharmacological doses they possess a similar effect to secretions of stomach and pancreas. Given intravenously, they generally inhibit the basal secretion of organs, stimulated by pentagastrin or pancreozymin, as well as the contraction of the gallbladder. Orally, calcitonin also suppresses by direct contact the secretion of the stomach. While calcitonin in higher doses shows only very slight and tolerable side effects (nausea, headache), somatostatin acts suppressively on many other hormone-regulated systems. Apart from this, disturbances of blood coagulation in monkeys and man were observed, findings which necessitate very careful application. Therapeutical trials appear reasonable with calcitonin in treating acute pancreatitis, in prophylaxis and treatment of stress ulcers with the danger of bleeding, in intensive care medicine, in preoperative procedure of Zollinger-Ellison syndrome as well as in duodenal ulcers (oral calcitonin). Double blind studies are carried out at present to answer most of these questions (acute pancreatitis, stress ulcers, duodenal ulcers), results of which should definitely be awaited.
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PMID:[Summary of work session 4: Effects of calcitonin and somatostatin on the stomach and pancreas--a possible therapeutic principle]. 82 14

To evaluate the effect of somatostatin in the treatment of acute pancreatitis, 63 patients were randomly allocated to continuous intravenous infusion for three days of 250 micrograms of somatostatin (Dura Scan, Odense, Denmark) per hour (n = 33), or placebo (n = 30). Patients with a first attack of pancreatitis, serum amylase level of more than 450 units per liter and symptoms for less than 24 hours were eligible for participation in the study. Apart from a slightly significant faster decrease in serum amylase concentrations, we were unable to demonstrate any significant benefit from somatostatin with regard to paraclinical values and clinical course.
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PMID:A double-blinded multicenter trial of somatostatin in the treatment of acute pancreatitis. 127 21

The experiments were performed on 34 dogs. The subcutaneous injection of boiled pancreatic juice was established to increase the survival of dogs in acute destructive pancreatitis (p < 0.001) and to decrease the specific volume damage to acinar (p < 0.01) and interstitial (p < 0.05) pancreatic tissue. It was also shown that boiled pancreatic autojuice exerted the therapeutic effect in chronic pancreatitis complicated by pancreatic fistulas. Five peptide components with a molecular mass from 4168 D to 1000 were discovered in the canine boiled pancreatic juice by liquid high pressure chromatography. Fractions with a molecular mass between 2187 and 1348 D were found to correspond to biologically active peptides, in particular to somatostatin. It is assumed that the therapeutic effect of boiled pancreatic juice used in acute pancreatitis may be due to somatostatin. Apparently pancreatic juice may turn an efficient therapeutic agent in acute pancreatitis and pancreatic fistulas.
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PMID:[Pancreatic juice peptides as possible regulators of reparative processes in the pancreas in acute and chronic pancreatitis]. 128 26

In vivo microscopy was performed to assess the effect of dextran 40, gabexate mesilate and somatostatin on the microcirculation in sodium taurocholate-induced pancreatitis in rats. Intraductal infusion of 0.4 ml of a 4% solution of sodium taurocholate decreased capillary blood flow, induced capillary stasis and increased vascular permeability in the head of the pancreas. Dextran 40, gabexate mesilate and somatostatin improved capillary blood flow in the initial phase of acute pancreatitis significantly and prevented stasis in 5 of 9, 3 of 8 and 7 of 10 (p < 0.05) cases. Only dextran 40 reduced the increase of vascular permeability. Decrease of capillary blood flow, capillary stasis and vascular permeability changes are important factors contributing to the pathogenesis of sodium taurocholate-induced pancreatitis. Dextran 40, gabexate mesilate and somatostatin exert a beneficial effect on the microcirculatory changes in this model of acute pancreatitis.
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PMID:The effect of somatostatin, gabexate mesilate and dextran 40 on the microcirculation in sodium taurocholate-induced pancreatitis. 128 68

A variety of receptors on pancreatic acinar and duct cells regulate both pancreatic exocrine secretion and intracellular processes. These receptors are potential sites of action for therapeutic agents in the treatment of pancreatitis. Cholecystokinin (CCK) receptor antagonists, which may reduce the level of metabolic "stress" on acinar cells, have been shown to mitigate the severity of acute pancreatitis in a number of models. Not all studies have shown a benefit, however, and differences may exist between different structural classes of antagonists. Because increased pancreatic stimulation due to loss of feedback inhibition of CCK has been proposed to contribute to the pain of some patients with chronic pancreatitis, CCK receptor antagonists could also be of benefit in this setting. Somatostatin and its analogs diminish pancreatic secretion of water and electrolytes and have been effective in treating pancreatic fistulas and pseudocysts. These agents are also being evaluated for their ability to reduce pain in chronic pancreatitis (perhaps by reducing ductal pressure by diminishing secretory volume) and mitigating the severity of acute pancreatitis (possibly by reducing the metabolic load on acinar cells). Recently described secretin receptor antagonists may also have therapeutic value as a means of selectively inhibiting pancreatic secretion of water and electrolytes.
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PMID:Receptor strategies in pancreatitis. 134 60


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