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)

The endocrine pancreatic tissue from patients with severe primary chronic pancreatitis (n=6). secondary chronic pancreatitis due to duct obstruction by carcinoma (n=6) and non-diabetic, non-pancreatitic controls (n=4) was studied qualitatively and quantitatively using specific immunocytochemistry and electron microscopy. Grouping of variously sized islets in the sclerotic tissue (sclerosis islets), islet neoformation by ductuloinsular proliferation, and intrainsular fibrosis were the main qualitative findings. Immunocytochemical quantitation of the distribution of insulin (B), glucagon (A), somatostatin (D) and pancreatic polypeptide (PP) producing cells revealed a significant relative increase in the number of A cells and a decrease in the number of B cells of the sclerosis islets in primary chronic pancreatitis ((B-44.1+/-9.3%:A-38.3+/-2.4%:D-8.6+/-5.1%:PP-4.6+/-4.1%) as well as in secondary chronic pancreatitis B-38.0+/-14.3%:A-38.4+/-19.0%:D-9.1+/-5.8%:PP-14.5+/-23.4%) compared with controls (B-71.1+/-8.1%:A-24.3+/-5.5%:D-8.0+/-2.8%:PP-0.5+/-0.4%). The number of PP cells was significantly increased in primary chronic pancreatitis only. It is suggested that scarring of the exocrine pancreas affects islet composition, probably by impairment of the local circulation and of glucose diffusion, thus leading to reduction of the number and glucose sensitivity of B cells. The hyperplasia of A and PP cells appears to be a secondary phenomenon due to the loss of B cells.
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PMID:The endocrine pancreas in chronic pancreatitis. Immunocytochemical and ultrastructural studies. 14 59

A reliable, sensitive, reproducible and specific radioimmunoassay for cholecystokinin-pancreozymin (CCK) has been developed, using rabbit antisera to highly purified porcine hormone. The natural occurring variant of CCK (39-CCK), in which the ordinary CCK is lengthened from its N-terminus by a hexapeptide, labelled with 125J, and repurified by column chromatography on Sephadex G-10 and on SP-Sephadex C-25, was used as tracer. Separation from antibody-bound labelled 39-CCK was carried out using a double antibody procedure. Non-specific interference with the assay system was abolished by ethanol extractions. Highly purified porcine CCK was used as standard. No significant crossreaction was found with gastrin, motilin, vasoactive polypeptide (VIP), gastric inhibitory polypeptide (GIP), natural and synthetic secretin, pancreatic glucagon or insulin. The sensitivity of the assay is approximately 40 pg/ml of test solution. The mean immunoreactive CCK concentration in 45 fasting normal subjects was 222 pg/ml increasing after food ingestion to 480 pg/ml. Somatostatin was able to abolish the stimulated CCK release. Elevated CCK concentrations were found in chronic pancreatitis. Immunohistochemical identification of pancreozymin cells was carried out either in surgical samples or in biopsy material. Approximately 1650 CCK cells per cross-section in the duodenum of humans have been found. The CCK cells usually appeared elongated, oval or pyramidal in shape and were observed to reach the lumen with their apical cell pole.
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PMID:Estimation of cholecystokinin-pancreozymin (CCK) in human plasma and tissue by a specific radioimmunoassay and the immunohistochemical identification of pancreozymin-producing cells in the duodenum of humans. 56 41

Oral glucose administration caused an exaggerated release of cross-reacting gastrointestinal glucagon-like immunoreactivity (GLI) and a slight early rise in immunoreactive glucagon (IRG) concentration in patients with chronic pancreatitis, who have impaired insulin release. Intravenous administration of 200 microgram of somatostatin, followed by infusion of 200 microgram over 2 1/2 h, abolished the GLI and insulin responses, but did not change glucose tolerance. This contrasts with the relatively minor effects of somatostatin on GLI responses in control subjects where the clear deterioration in glucose tolerance may relate to inhibition of insulin release.
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PMID:Inhibition of exaggerated gastrointestinal glucagon responses in chronic pancreatitis by somatostatin. 59 21

Unmodified synthetic somatostatin, given as a 200-microgram intravenous bolus, plus 200 microgram infused over 3 hours, had no effect on basal plasma insulin and pancreatic glucagon-like immunoreactivity (GLI) levels, both in controls and in patients with chronic pancreatitis. Somatostatin inhibited insulin-hypoglycaemia-induced pancreatic GLI release in controls and in patients with pancreatitis, and prolonged the insulin-induced fall in blood glucose in the patients. Arginine, presumably via insulin release, caused a fall in free fatty acids (FFA) in controls, which was inhibited by somatostatin. Somatostatin abolished the rebound rise in plasma FFA in patients with pancreatitis after insulin-hypoglycaemia. This effect may be related to inhibition of pancreatic GLI release or may be a direct action of somatostatin on lipolysis.
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PMID:The effects of somatostatin on hormonal and metabolic responses in chronic pancreatitis. 89 37

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

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

In a prospective clinical-experimental study, 15 patients with chronic pancreatitis operated consecutively due to severe pain were examined for the effects of a duodenum-preserving resection of the pancreas head on endocrine pancreas function. This was done by means of oral and intravenous glucose tolerance testing before the operation, on the 10th or 11th postoperative day, and three months after the operation. In addition to glucose levels in the peripheral venous blood, levels of insulin, C-peptide, glucagon, somatostatin, and pancreatic polypeptide were determined. As indicated by the k-value, glucose tolerance improved postoperatively in 11 patients; two patients showed no change, and one patient was worse. Only one patient developed evident diabetes mellitus immediately postoperatively. The pre- and postoperative levels of insulin and C-peptide showed no significant differences. The fasting levels of glucagon were significantly lower postoperatively than before the operation (2p less than 0.01). Duodenum-preserving pancreas head resection led to improvement of the glucose tolerance in the majority of patients; a deterioration was observed only in two cases.
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PMID:[The effect of duodenum-preserving pancreatic head resection on the endocrine pancreas function in patients with chronic head pancreatitis]. 134 82

Pancreatic ascites is an entity defined as amylase levels up to 1.000 U/l in ascitic liquid. Frequently, it is secondary to a rupture of pancreatic ductus or pseudocyst and foreward communication to peritoneal space. We present a male diagnosed of calcified alcoholic chronic pancreatitis with pancreatic ascites secondary to a pseudocyst. Combination of parenteral nutrition and sintetic cyclic somatostatin was efficient. It would act by reducing pancreatic secretion in a long-term manner, which is the final purpose of the treatment. This association would be considered as a former tool in ascitic pancreatic patients, evacuatory punction or delayed surgery been relegated to a conservatory treatment failure or when primary pathology indicate it.
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PMID:[Treatment with somatostatin of pancreatic ascites]. 135 7

The prophylactic effect of perioperative use of somatostatin on postoperative increase of pancreatic digestive enzymes was investigated in this double blind, randomized study. Thirty three patients undergoing pancreatic surgery because of chronic pancreatitis were divided randomly into two groups. Fifteen patients received somatostatin- (dose 125 micrograms/hour), 18 placebo-infusion, pre- and postoperatively for a total time of 48 hours. The level of serum amylase, lipase, gammaGT, calcium, creatinine and blood glucose was determined every 12 hours. In the placebo group the serum lipase and amylase increased significantly (p less than 0.001), while the calcium decreased. In the somatostatin treated patients only the lipase level increased significantly (p less than 0.01), while the amylase and calcium showed no significant changes compared to their initial values. The postoperative increase in serum enzyme levels is interpreted as being an indicator of pancreatic injury. These results suggest that the perioperative use of somatostatin has beneficial effect for the prevention of pancreatic enzymes increases, associated with pancreatic surgery or its complications in patients with chronic pancreatitis.
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PMID:[Somatostatin in the prevention of postoperative increase of pancreatic enzyme after pancreatic surgery]. 137 31

Somatostatin, originally detected by Krulich and ultimately isolated by Brazeau, was initially described as a growth hormone release-inhibiting factor. Subsequent investigation into the use of native somatostatin and the development of long-acting somatostatin analogues, especially octreotide acetate, have fostered increasing uses of these compounds. Though the clinical and investigational uses of somatostatin and its analogues are varied, one central theme remains constant: the ability of these agents to suppress circulating peptide levels. This article, a review of the current non-endocrine applications of somatostatin and its analogues, covers a wide range of potential applications for somatostatin-like compounds. These include use in cirrhosis and variceal bleeding, peptic ulcer disease, pancreatic fistulas, acute and chronic pancreatitis, dumping syndrome, cancer therapy, small bowel fistulas, psoriasis, pain control, and autonomic hypotension. Somatostatin may also play a role in the development and potential treatment of neurologic disease and may have profound found influence on behavior.
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PMID:Non-endocrine applications of somatostatin and octreotide acetate: facts and flights of fancy. 168 32


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