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)

Glucagon-like peptide-1(7-36)amide [GLP-1(7-36)amide], a new important incretin candidate, binds to specific high-affinity receptors on rat insulinoma-derived beta-cells (RINm5F). In the present study, the effect of somatostatin-14 on the GLP-1(7-36)amide-induced insulin release and cAMP generation in this cell line was investigated. Somatostatin did not decrease basal insulin release of RINm5F cells. The GLP-1(7-36)amide-induced insulin release was decreased concentration dependently by somatostatin. Somatostatin, 1 microM reduced the maximally GLP-1(7-36)amide-stimulated (0.1 microM) insulin release to basal insulin levels. The GLP-1(7-36)amide-induced cAMP production was significantly decreased by somatostatin in a concentration-dependent manner. The GLP-1(7-36)amide concentration causing half-maximal cAMP production was 2.98 +/- 1.56 nM. Somatostatin left the EC50 unaltered but decreased the maximal GLP-1(7-36)amide effect for 32% in the presence of 1 nM somatostatin and for 50% at 1 microM. In additional experiments, the interaction of both hormones was evaluated in the perfused pancreas as a nontumor model. Somatostatin (1 nM, 1 microM) inhibited the glucose-induced (6.7 mM) and GLP-1(7-36)amide-potentiated (0.05, 0.5, and 5 nM) insulin release dose dependently. The biphasic pattern of insulin release remained preserved. The GLP-1(7-36)amide-induced insulin release is potently inhibited by somatostatin-14. This effect was demonstrated in different model systems for beta-cell function studies. The present data allow the conclusion that the somatostatin action upon GLP-1(7-36)amide effects is at least partly related to regulation of intracellular cyclic nucleotides.
Pancreas 1989
PMID:Interaction of glucagon-like peptide-1(7-36)amide and somatostatin-14 in RINm5F cells and in the perfused rat pancreas. 257 56

Somatostatin (SST) is used in the treatment of acute pancreatitis (AP) to inhibit pancreatic exocrine secretion, which represents one of the goals of medical treatment in this disease. Its therapeutic efficacy, however, is poor. One hypothesis, which has not yet been investigated, is that i.v. SST might be broken down by blood proteolytic enzymes. In order to evaluate the structural integrity and biological activity of infused SST, somatostatin-like immunoreactivity (SLI) and levels of pancreatic enzymes were monitored in the blood stream during the infusion of SST-14 (3,5 micrograms/kg/h for 48 h) in eight patients with severe acute pancreatitis. SLI was measured by both radioimmunoassay (RIA) and high-pressure liquid chromatography (HPLC). The results indicate that SLI levels increase promptly after the beginning of infusion, with a slower increase between 6 and 36 h, and a rapid increase again at 48 h. HPLC analysis shows a single peak of SLI with the same retention time as standard SST-14. Total amylase, lipase, and trypsinogen significantly decreased compared with pretreatment values (48, 63.1, and 77.4%, respectively) after 24 h of SST infusion, while a decrease in elastase 1 (62.6%) was observed later at 48 h. These results indicate that in severe AP, somatostatin recovered in plasma retains its biological activity: it inhibits pancreatic circulating enzymes, an action not influenced by breakdown of the peptide, as demonstrated by HPLC of the SLI measured in plasma.
Pancreas 1989
PMID:Somatostatin infused during acute pancreatitis retains its biological activity. 257 57

Atrial natriuretic factor (ANF) binding sites in adult rat exocrine pancreas were studied by autoradiography using slide-mounted frozen tissue sections with mono-iodinated ANF (101-126) as the tracer. Radiolabel was displaced by unlabeled atrial peptide (IC50 = 2 X 10(-11) M). High specific labeling was found in pancreatic acini. The presence of endogenous ANF has also been demonstrated in the exocrine pancreas by immunocytochemistry on ultra-thin sections obtained by cryoultramicrotomy. ANF-like immunoreactivity was found in acinar and centro-acinar cells as well as cells of the intercalated duct. For these cells, immunostaining was observed at the plasma membrane level, in the cytoplasm and nucleus. In the cytoplasm, ANF-like immunoreactivity was observed in the cytoplasmic matrix, mitochondria, and zymogen granules. In the nucleus, ANF-like immunoreactivity was distributed in the vicinity of the heterochromatin region primarily in the euchromatin. It was also detected in the plasma membrane of microvilli of acinar and duct cells, and in the lumen of secretory ducts. In centro-acinar cells, the reaction product was also found sparsely at the nuclear envelope. No immunoreactivity was observed when anti-human ANF serum preincubated with rat ANF was used. No modifications were observed when this antiserum was preincubated with heterologous peptides (NPY, CRF, GRF, TRH, somatostatin). These data provide autoradiographic evidence of ANF binding sites, indicate the presence of this peptide in acinar and centro-acinar cells as well as cells of the intercalated duct, and immunocytochemical evidence for the internalization of endogenous ANF by exocrine pancreas.
Pancreas 1987
PMID:Atrial natriuretic factor and exocrine pancreas: autoradiographic localization of binding sites and ultrastructural evidence for internalization of endogenous ANF. 281 60

Surgical fragments of healthy and tumor-bearing pancreas from a patient with pancreatic tumor were studied by electron or light microscopy, histochemistry, and immunocytochemistry (human insulin, glucagon, somatostatin, gastrin, and bovine pancreatic polypeptide). Histological results were compared to those obtained by radioimmunoassay, both in tumor and serum. The tumor was identified as a glucagonoma because reactions for Grimelius' silver impregnation and immunoreaction with an antiserum against glucagon were positive and because a very high level of glucagon in the tumor was observed. Insulin, somatostatin, and gastrin levels remained normal, both in tumor and serum, but the glucagon level was normal in serum. Associated with this silent glucagonoma, an uncommon nesidioblastosis was also diagnosed with many A cells irregularly mixed with acinar cells, isolated or clustered in small groups. Acinar "intermediate" cells of "A" type were also observed. Such associative histopathological processes evoked possible development of an endocrine tumor from nesidioblastic-like tissue. Its embryogenic origin remained uncertain.
Pancreas 1988
PMID:Silent human pancreatic glucagonoma and "A" nesidioblastosis. 285 84

The amounts of insulin, glucagon and somatostatin in the pancreas of NOD mice were determined and the results were compared with those of normal ICR-strain mice, and plasma antibodies to Coxsackie B-3 and reovirus types 1, 2 and 3 were measured. In the pancreas of NOD mice with fasting plasma glucose (FPG) less than 140 mg/100 ml, the insulin content of the male mice was similar to that of the normal controls, ranging to 3.55 +/- 0.31 U/g wet weight of pancreas, but it was already significantly decreased to 0.85 +/- 0.52 U/g in the female mice. In the NOD mice with FPG more than 201 mg/100 ml, it was 0.002 +/- 0.001 U/g. The glucagon content of the pancreas was 7.76 +/- 0.89 micrograms/g in the normal controls and it was decreased slightly in the NOD mice, but the values among the NOD mice were not significantly different. Pancreas somatostatin showed a tendency to be higher in the NOD mice with FPG more than 201 mg/100 ml. Histologically cell infiltration into the pancreatic islets was conspicuous in the hyperglycemic NOD mice, but it was found even in the normoglycemic NOD. Plasma antibodies to Coxsackie B-3 Virus and reovirus types 1, 2 and 3 were not detected at any stage of FPG.
 ...
PMID:Insulin, glucagon and somatostatin content of the non-obese diabetic (NOD) mouse pancreas and plasma virus antibodies to Coxsackie B- and reoviruses. 286 17

We determined the effects of exogenous somatostatin-14 (100 and 200 ng/kg/h; mimicking postprandial somatostatin concentrations) on pancreatic responses to a background infusion of secretion in combination with graded doses of CCK-8 in conscious dogs with chronic gastric and duodenal fistulas. The lower dose of somatostatin-14 (S-14), which produced S-14 plasma levels lower than measured after a meal, did not change basal or stimulated pancreatic secretion. The upper dose of S-14, which produced plasma S-14 concentrations slightly above the postprandial range, caused inhibition of pancreatic fluid and protein secretion to low doses of CCK-8 (p less than 0.05). The inhibition was surmountable with higher doses of CCK-8. We interpret these data as indicating that circulating S-14 is not an important hormonal regulator of exocrine pancreatic secretion.
Pancreas 1986
PMID:Effect of circulating somatostatin on exocrine pancreatic secretion in conscious dogs. 288 2

A 41-year-old woman with metastatic glucagonoma and the characteristic disabling rash, necrolytic migratory erythema, was treated with a synthetic somatostatin analog while waiting to undergo curative surgical resection. Plasma glucagon concentration (1,500-3,300 pg/ml, normal less than 200) remained elevated during analog therapy as the rash cleared. Only with surgical resection (partial pancreatectomy and partial hepatectomy) did glucagon levels return to normal. The therapeutic benefit caused by the analog in this syndrome differs from that in other endocrine tumor syndromes such as pancreatic cholera, carcinoid, or gastrinoma where circulating levels of tumor-produced agents are suppressed in conjunction with control of symptoms.
Pancreas 1986
PMID:Somatostatin analog-induced remission of necrolytic migratory erythema without changes in plasma glucagon concentration. 288 3

The pathophysiological, biochemical, histological, ultrastructural, and immunohistochemical characters of a case of malignant pancreatic islet cell tumor with watery diarrhea syndrome were carefully investigated. Four hormones or mediators--somatostatin (SST), vasoactive intestinal peptide (VIP), serotonin, and prostaglandin E--were markedly elevated in the circulation. The diagnosis was further confirmed by exploratory laparotomy and autopsy. The contents of SST and VIP in tumor tissues were very high. Gel chromatography of tumor extract revealed single peaks for both SST and VIP. Immunohistochemical studies of tumor tissues showed numerous immunoreactive cells to anti-SST, moderate amount of VIP-positive cells, and a few hCG-, insulin-, and glucagon-positive cells. In conclusion, this is an unusual case of Verner-Morrison syndrome in which three kinds of bioactive hormones or mediators were simultaneously secreted; peptides, amine, and prostaglandin.
Pancreas 1986
PMID:Watery diarrhea syndrome caused by multihormonal malignant pancreatic islet cell tumor secreting somatostatin, vasoactive intestinal peptide, serotonin, and prostaglandin E--a clinicopathological, biochemical, immunohistochemical, and ultrastructural study. 288 47

In a 30-year-old man, a total external pancreatic fistula developed after enucleation of an insulinoma of the head of the gland. The output of the fistula was reduced to some extent by total parenteral nutrition. Much greater reductions of volume were noted during short-term administration of two somatostatin preparations, SMS 201-995 and Somatofalk, for 1 week consecutively. Although the former showed several advantages over the latter drug, such as absence of an escape phenomenon and of a rebound effect, neither drug caused a closure of the fistula. Spontaneous closure of the fistula occurred after 3 1/2 months.
Pancreas 1986
PMID:A comparison of the effects of two somatostatin analogues in a patient with an external pancreatic fistula. 288 48

The effect of increased doses of Somatostatin-14 (3, 10, 30, 100, 300 micrograms/h) on basal release of insulin, pancreatic glucagon and pancreatic polypeptide (PP) was investigated on eight normal volunteers. Levels of Somatostatin-like immunoreactivity (SLI) was determined in order to correlate the increased SLI levels with the degree of islet hormone inhibition (r = 0.9947, p less than 0.01). By increasing the basal levels of SLI by one-third, a significant inhibition (p less than 0.01) of insulin, glucagon, and PP was noted (78.5, 78.6, 75.2%, respectively, on basal levels). The maximal effect was obtained with 300 micrograms/h for insulin, with 30 micrograms/h for glucagon and 100 micrograms/h for PP. In evaluating the relative inhibitory potency of somatostatin, expressed as ED50, the theoretic potency of somatostatin on each peptide had similar values, ranging from 30 to 10 micrograms/h. The present data show that a minimal peripheric increase in SLI is able to regulate basal islet pancreatic hormones.
Pancreas 1987
PMID:Dose-response effect of somatostatin-14 on human basal pancreatic hormones. 289 Jan 57


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