Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 45-year-old man was operated for surgical treatment of a long-standing peptic ulcer disease and upon inspection of the pancreas for suspected Zollinger-Ellison syndrome, tumor nodules were found in this organ. The tumor tissue examined by immunofluorescence showed specific staining only after incubation with anti-pancreatic polypeptide. Negative results were obtained with antisera directed against insulin, pancreatic glucagon, somatostatin, GLI, VIP, secretin, and gastrin. Examination of the tissue by electron microscopy revealed a homogeneous population of small granule-containing cells. This case, therefore, illustrates a tumor composed of one single hormone-producing cell type and allows definition of the ultrastructural features of human pancreatic polypeptide-containing cells.
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PMID:Human islet cell tumor storing pancreatic polypeptide: a light and electron microscopic study. 37 22

Sections of gastric mucosa removed during surgery for cancer or peptic ulcer and containing regions of intestinal metaplasia were studied by the immunofluorescence technique using several antiserums against intestinal hormones. Endocrine cells such as cells containing somatostatin, glicentin (gut GLI-I), motilin, and probably cholecystokinin were found within metaplastic intestinal epithelium while secretin and neurotensin, which are present in the normal intestinal mucosa, were not detected in metaplastic epithelium. The endocrine-cell population present in the intestinal metaplasia resembles that found in the cryptal region of the normal small intestine, a finding in accordance with the fact that intestinal metaplasia of gastric mucosa usually reproduces structural and histochemical characteristics of small intestinal crypts.
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PMID:Endocrine cells in the intestinal metaplasia of gastric mucosa. 47 6

Effects of somatostatin on extrapancreatic glucagon secretion in totally depancreatized dogs were examined. Somatostatin infusion at a rate of 3 microgram/min showed a rapid decrease of total glucagon-like immunoreactive materials (total GLI) measured by nonspecific antiserum, AGS 10, and gut glucagon immunoreactivity (gut GI) measured by specific antiserum, AGS 18, in systemic blood. Gut GLI calculated as the difference between total GLI and GI did not decrease significantly within 30 min. No changes of blood glucose were noted. Significant decreases of all glucagon fractions were observed when the rate of somatostatin infusion was increased to 10 microgram/min and prolonged for 90 min, whereas again blood glucose did not change at all. It is concluded that somatostatin inhibits both gut GI and GLI secretion, although gut GLI remains in circulation longer than gut GI. Suppression of gut GI is not effective for the reduction of blood glucose once an extreme hyperglycemia is brought about by insulin deficiency.
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PMID:Failure of somatostatin to decrease blood glucose by suppression of extrapancreatic glucagon in severely diabetic depancreatized dogs. 75 98

The effects of somatostatin on GLI release during the absorption of intraduodenally administered glucose, casein hydrolysate and longchain triglycerides were studied in conscious dogs. Whereas, after an intraduodenal glucose load, GLI rose promptly in saline-infused control experiments to a peak of 5 ng/ml (SEM +/- 4) in 60 minutes, significantly lower values were observed during somatostatin infusion (P less than 0.025 -- 0.05). A similar reduction in the magnitude of the GLI response to intraduodenally administered casein hydrolysate (P less than 0.05) and fat (p less than 0.05) was observed.
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PMID:The effect of somatostatin on the response of GLI to the intraduodenal administration of glucose, protein, and fat. 118 67

We previously reported that sulfonylurea treatment reduces insulin (IRI), glucagon (IRG) and somatostatin (SRIF) release following metabolic stimuli from the isolated perfused pancreas of normal rats and that a reduction in IRI, IRG and SRIF pancreatic content was also observed. The present work was undertaken to investigate the effects of long-term glibenclamide treatment on the gastrointestinal content of gut hormones in normal rats. Moreover, the effects of sulfonylurea treatment on IRI, IRG, and SRIF pancreatic content were also analyzed and compared to the peripheral hormone plasma levels. Two groups of male Sprague-Dawley rats received glibenclamide (1 mg/kg/day per os; n = 14) or placebo (distilled water; n = 10) for 5 months, respectively. Tissue contents of IRI, IRG and SRIF in acid-ethanol extracts of pancreas and of gastric inhibitory peptide (GIP), vasoactive intestinal polypeptide (VIP), entero-glucagon (gut-GLI) and SRIF in acid-ethanol extracts of intestine were determined. Blood glucose and plasma pancreatic hormone levels were also measured. Glibenclamide treatment lowered the levels of IRI, IRG and SRIF in the pancreatic tissue; in the same way gut-GLI, SRIF and VIP intestinal concentrations were significantly reduced, whereas no significant inhibition was detected in intestinal GIP content. Blood glucose levels and IRI and SRIF plasma concentrations were similar in the two groups. IRG plasma levels were reduced in the sulfonylurea group. These findings might suggest that sulfonylurea suppresses hormone biosynthesis in a non-specific manner.
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PMID:Effects of long-term glibenclamide administration on gastrointestinal and pancreatic hormones in normal fasting rats. 249 27

The concentrations of immunoreactive components of glucagon, somatostatin, substance P, and vasoactive intestinal polypeptide (VIP) in the brain, stomach, and gut of the neotenic Mexican axolotl (Ambystoma mexicanum) were determined by radioimmunoassay using antibodies of defined regional specificity. The molecular forms of the immunoreactive components were analyzed by high-performance liquid chromatography (HPLC). The concentrations and molecular forms of somatostatin and VIP in axolotl brain were comparable to the concentrations in mammals but the substance P-like immunoreactivity was resolved by HPLC into components with the retention times of physalaemin and substance P together with their oxidized forms. No glucagon-like material was detected in the axolotl brain. The concentrations of substance P and VIP in the A. mexicanum digestive tract were appreciably lower than in the mammalian digestive tract and the VIP-like material did not coelute with porcine VIP. Somatostatin-14 represented the major molecular form in the axolotl stomach and gut. The distribution and molecular properties of the glucagon-like peptides in the axolotl digestive system were markedly different from these parameters in mammalian gut. Glucagon-like material is present only in low amounts in porcine and human stomach and, the concentration of enteroglucagon (N-GLI) in the gut is at least fiftyfold greater than pancreatic glucagon (C-GLI) concentrations. The axolotl stomach, in contrast, contains high levels of glucagon-like immunoreactive material and, in both stomach and gut, the levels of C-GLI and N-GLI were comparable. The glucagon-like material was heterogeneous on HPLC and was resolved into two major components but no component with the retention time of mammalian glucagon was present.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulatory peptides (glucagon, somatostatin, substance P, and VIP) in the brain and gastrointestinal tract of Ambystoma mexicanum. 258 Jul 53

The prevalence of endocrine differentiation of conventional gastric adenocarcinoma was evaluated on the 212 cases (including 62 mucosal carcinomas) of consecutively resected stomach for adenocarcinoma in our hospital using anti-chromogranin A (CGA) antibodies. CGA-positive cells were found in 28 of 150 cases (18.7%) as an integral tumor component. In immunocytochemistry and electron microscopic examinations, we could classify these 28 cases into three groups according to the distribution patterns of CGA-positive cells. The first group consisted of 12 cases in which scattered CGA-positive cells were located in neoplastic glands. The second group consisted of six cases of scirrhous carcinoma in which CGA-positive cells were separated by fibrovascular tissue. The third group consisted of ten cases in which the positive cells were present in clusters. No definite correlation was recognized between the appearance of CGA cells and histologic types of predominance. In the analysis of the hormonal substances coexpressed by CGA-positive cells, immunoreactive serotonin (SER) was found most frequently, and somatostatin (SS), gastrin (GAS), glucagon/glicentin (GLU/GLI), and peptide-tyrosine-tyrosine (PYY) like immunoreactivities were found in a few tumor cells. CGA-positive cells occupied limited parts of the tumors in most cases, and they were noticeably more frequent in advanced stage cases. This might explain why endocrine differentiation reflects the dysexpression of the neoplastic stem cells. Furthermore, absence of mitotic figures in this type of cell and negativity of a single colony composed exclusively of CGA cells in metastatic foci suggested that these cells are in a dormant phase and are probably postmitotic.
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PMID:Endocrine differentiation of gastric adenocarcinoma. The prevalence as evaluated by immunoreactive chromogranin A and its biologic significance. 304 73

Based on the assumption that somatostatin may inhibit peptide release through junctional complexes or through local circulation, an immunfluorescent technique for somatostatin and GLI in the gut was applied in order to investigate whether suppression of GLI release by i.v. administration of somatostatin was a physiological effect of somatostatin or not. Somatostatin-immunoreactive cells (GIF-cells) in the human and canine intestine had no direct cellular contacts with GLI-immunoreactive cells (GLI-cells). This finding suggests that somatostatin in the intestine does not inhibit GLI release through junctional complexes between GIF- and GLI-cells. As to the local circulation, most of GIF-cells in the canine intestine were distributed in the deeper portion of the intestinal gland which corresponds to the upstream sides of the local blood supply of the intestinal gland, as reported by REYNOLD et al. The ratio of GIF-cells to total cells (GIF-cells + GLI-cells) was 68% in the duodenum and 25% in the ileum. In contrast a limited number of GIF-cells was found in the human duodenum where a few GLI-cells were distributed and a few GIF-cells were seen in the human ileum where a large number of GLI-cells were located. Findings in the dog suggest the possibility that somatostatin inhibits GLI release from GLI-cells through the local circulation system of intestinal glands. However, findings in humans suggest that the same possibility does not apply to the human gut. Differences of population density of intestinal GIF-cells between humans and dogs indicate that the functional meaning of GIF-cells may vary from one species to another.
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PMID:Does somatostatin in the gut inhibit the GLI release locally? 610 41

In normal fasting ducks, a somatostatin infusion (800 ng/kg/min for 30 min) elicited a prompt inhibition of insulin secretion, plasma levels falling from 140 +/- 20 to 20 +/- 6 pg Eq/ml as observed in mammals.--However plasma glucagon-like-immunoreactivity shown to be decreased in mammals by somatostatin was sharply increased from a mean basal level of 1.46 +/- 0.13 ng Eq/ml to 6.61 +/- 0.77 ng Eq/ml. This effect was not mediated via inhibition of growth hormone secretion since it was also observed in hypophysectomised ducks. Despite the fall in plasma insulin and rise in GLI observed with somatostatin infusion in intact birds, plasma glucose concentrations were lower than with control saline infusion.
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PMID:Somatostatin stimulates glucagon secretion in ducks. 610 14

To characterize the glucagon released in response to epineephrine in depancreatized dogs, plasma samples before and during epinephrine infusion were subjected to molecular-sieve chromatography on Bio-Gel P-30 columns. The chromatographic profile for extrapancreatic immunoreactive glucagon (eIRG) revealed two glucagon moieties of molecular weight 9,000 to 12,000. GLI of this molecular weight was released in response to epinephrine only under conditions of prevailing hyperglycemia. To determine if glucagon's participation in epinephrine-induced hepatic glucose overproduction in diabetes was dependent upon the degree of metabolic control, six conscious depancreatized dogs were infused with epinephrine or epinphrine plus somatostatin, under conditions of prevailing hyperglycemia or normoglycemia. Under normoglycemic conditions, epinephrine stimulated eIRG release, but there was a similar rise in hepatic glucose production (Ra) with or without glucagon suppression by somatostatin. Under hyperglycemic conditions, epinephrine stimulated eIRG and GLI release, and the rise in Ra was significantly greater with epinephrine than with epinephrine plus somatostatin infusion. Thus, under conditions of good metabolic control, epinephrine increased hepatic glucose production independently of glucagon, whereas with poor metabolic control, glucagon contributed to hepatic overproduction of glucose.
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PMID:Chromatographic pattern of extrapancreatic glucagon and glucagon-like immunoreactivity before and during stimulation by epinephrine and participation of glucagon in epinephrine-induced hepatic glucose overproduction. 611 73


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