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)

Gut endocrine cells in a total of 18 gastric adenocarcinomas in inbred Wistar rats induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and gastrin or serotonin, were examined histologically, ultrastructurally, and immunohistochemically for gastrin, somatostatin, calcitonin, glicentin, and serotonin. A large number of argyrophil cells were observed in 17 tumors (94.4%) and 14 tumors (77.8%) had argentaffin cells. Immunohistochemically, C-terminal fragment of gastrin (G17) immunoreactivity was observed in 15 (82.2%) out of the 18 tumors, but 3 G17-positive tumors had no G 34 immunoreactive cells in rats treated with MNNG plus gastrin. Serotonin immunoreactivity was detected in 14 tumors (77.8%). Somatostatin immunoreactivity was detected in 7 of the 11 tumors (63.6%) in rats treated with MNNG plus gastrin whereas no tumor in rats treated with MNNG plus serotonin had somatostatin, the difference of the incidence being significant (P less than 0.05). One endocrine cell carcinoma which consisted mainly of serotonin-producing cells was observed in a rat treated with MNNG plus serotonin. Calcitonin and glicentin immunoreactivity was not demonstrated in any tumors. Ultrastructurally, three types of endocrine granule were found in the tumor cells. These data suggest that hormonal environment in stomach carcinogenesis may influence the expression of endocrine cells within the tumors.
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PMID:Gut endocrine cells in rat stomach carcinoma induced by N-methyl-N'-nitro-N-nitrosoguanidine. 287 Oct 28

Calcitonin- and serotonin-storing cells have been immunocharacterized in prostate gland, urethra, urinary bladder and anal canal. In addition, a few hCG and somatostatin immunoreactive cells have been detected in prostate gland. All these cells were dispersed throughout the epithelial lining. In the anal canal, calcitonin cells were exclusively confined to the anal ducts and anal transitional zone epithelium. Calcitonin and serotonin cells were seen in some examples of prostatic adenocarcinoma. Combined techniques most often showed coexistence of calcitonin and serotonin immunoreactivities in the same endocrine cell. hCG immunoreactive cells corresponded to a subpopulation of serotonin-, calcitonin-storing cells. Calcitonin and serotonin cells were present in most organs which originated from the cloaca. In this territory, this distinctive endocrine pattern could be regarded as an excellent marker of cloacal derived tissues. These tissues constitute an additional site for extrathyroid C-cells. It is likely that calcitonin cells are a component of some prostatic adenocarcinomas.
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PMID:Calcitonin immunoreactive cells in prostate gland and cloacal derived tissues. 287 50

Calcitonin (CT) binds to specific receptors in the hypothalamus and has been localized in the pituitary, suggesting a potential neuroendocrine role for this peptide. We and others have previously shown that CT given centrally markedly suppresses pulsatile GH secretion. However, the mechanism mediating this response remains to be elucidated. In the present study, we assessed the involvement of the two hypothalamic GH-regulatory peptides, somatostatin (SRIF) and GH-releasing factor (GRF), using a combination of in vivo and in vitro techniques. Six-hour GH secretory profiles were obtained from eight groups of freely moving rats bearing chronic intracerebroventricular (icv) and intraatrial cannulae. In four groups, salmon (s) CT (250 ng/10 microliters) was administered icv, whereas the remaining four groups received either normal saline (NS) icv or sCT iv. Central injection of sCT caused a severe suppression in amplitude of spontaneous GH pulses compared to NS icv-treated control rats, whereas the same dose of sCT iv had no significant effect. Passive immunization of sCT icv-injected rats with a specific antiserum to SRIF failed to restore the amplitude of GH pulses to normal values. In addition, in vitro basal and 50 mM K+-stimulated SRIF release from incubated hypothalamic fragments was not altered by sCT in doses ranging from 10(-10) to 10(-6) M. The iv administration of a bolus of rat GRF (1-29)NH2 (1 microgram) 1 h after sCT icv injection also failed to augment plasma GH levels compared to sCT iv-treated rats (16.6 +/- 10.0 vs. 326.6 +/- 63.6 ng/ml; P less than 0.001) and NS icv controls (407.2 +/- 145.4 ng/ml; P less than 0.01). Blood calcium levels decreased similarly 1 h after iv and icv sCT administration. These results demonstrate that: sCT inhibits pulsatile GH secretion via a central nervous system site of action, GH suppression induced by sCT is apparently not due solely to increased hypothalamic SRIF release, and centrally administered sCT produces an acute loss of responsiveness of somatotrophs to GRF, which can be dissociated from peripheral blood calcium levels.
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PMID:Mechanisms of calcitonin-induced growth hormone (GH) suppression: roles of somatostatin and GH-releasing factor. 288 73

Mouse-Chinese hamster hybrids segregating mouse chromosomes were analyzed by Southern hybridization techniques to map the genes for somatostatin (Smst), glucagon (Gcg), calcitonin (Calc), and parathyroid hormone (Pth). The mouse gene for somatostatin, detected on a 20-kb EcoRI fragment, is located on mouse chromosome 16. Glucagon cDNA hybridized to a 14-kb EcoRI fragment residing on chromosome 2. Calcitonin and parathyroid hormone genes, detected on 7.8-kb HindIII and 6.0-kb BamHI fragments, respectively, were on mouse chromosome 7. The calcitonin and parathyroid hormone genes appear to be part of a larger linkage group which has been conserved in mouse and man.
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PMID:Mapping polypeptide hormone genes in the mouse: somatostatin, glucagon, calcitonin, and parathyroid hormone. 288 56

Calcitonin gene-related peptide (CGRP) exists in nerves throughout the gastrointestinal tract and pancreas, and exogenous CGRP has been reported to inhibit many endocrine and exocrine secretions of the gut and pancreas. Because somatostatin also has widespread inhibitory actions and because both gut and pancreatic somatostatin secretion may be under peptidergic control, we examined the influence of CGRP on circulating levels of somatostatin-like immunoreactivity (SLI) and on hormone output from the duodenal lobe of the dog pancreas in situ. Intravenous infusion of human CGRP in anesthetized dogs increased arterial SLI in a dose-dependent manner. During iv infusion of CGRP at 500 pmol/min, the increment of circulating SLI (change at 20 min, +175 +/- 24 fmol/ml) was composed of nearly equimolar amounts of SLI-14 and SLI-28, suggesting an effect of CGRP on both gastric and intestinal somatostatin secretion. The effect of iv CGRP (500 pmol/min) on arterial SLI exceeded those of iv CCK-8 (440 pmol/min), iv isoproterenol (10 nmol/min), and intragastric administration of acidified liver extract. In contrast, salmon calcitonin (500 pmol/min, iv) was without effect. CGRP did not stimulate pancreatic SLI output when infused iv (500 pmol/min) or when infused directly into a pancreatic artery (5 pmol/min). The pancreatic infusion of CGRP decreased insulin output slightly (change at 20 min, -21 +/- 8%), but did not affect glucagon output. We conclude that CGRP is a most effective yet selective stimulator of gastrointestinal somatostatin release, with little influence on islet function. We suggest that exogenous and possibly endogenous neuronal CGRP could exert inhibitory effects on gastrointestinal function via the release of somatostatin.
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PMID:Calcitonin gene-related peptide: a potent and selective stimulator of gastrointestinal somatostatin secretion. 288 97

The authors compared the effect of synthetic salmon calcitonin and synthetic somatostatin (SRIF) and hypercalcaemia on an oral glucose tolerance test (OGTT) in healthy subjects in relation to changes of insulin (IRI), somatotrophin (HGH) and cortisol levels. Calcitonin--100 U--in an intravenous infusion in the course of OGTT markedly altered the pattern of the blood sugar curve and of IRI levels. After the initial retardation of the rise of the blood sugar and IRI levels during the 15th and 30th min, the values of both variables increased parallel during the 120th and 180th min, as compared with the control examination after saline. SRIF--500 micrograms--administered in an intravenous infusion altered the pattern of the blood sugar and IRI curves in a similar way as calcitonin, however during the 120th and 180th minute when the blood sugar levels rose significantly the IRI levels did not rise. The curve of HGH levels on infusion with calcitonin displayed a typical three-phase course, as during the control OGTT. During infusion of SRIF the HGH levels were insignificantly but constantly reduced during the first 60 mins. of the OGTT and thus the typical three-phase shape of the curve was impaired. Calcitonin significantly raised the cortisol levels throughout the OGTT, while SRIF caused their slight decline during the 120th min. Hypercalcaemia induced by infusion of 13.3 mg Ca/kg body weight did not alter significantly the blood levels of glucose, IRI and HGH, but caused a significant rise of the cortisol level throughout the OGTT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of calcitonin, somatostatin and hypercalcaemia on metabolic and hormonal indicators during an oral glucose tolerance test (OGTT). 288 8

Calcitonin gene-related peptide occurs in intrapancreatic nerves and endocrine cells. The peptide is therefore a candidate for being of physiological importance for pancreatic function. We examined the direct effects of calcitonin gene-related peptide on islet hormone secretion in the pig by infusing the peptide into the superior pancreatic artery. We found that 15 min intrapancreatic infusion of calcitonin gene-related peptide (22 pmol/min) decreased baseline pancreatic insulin output from 48 +/- 10 microU/min to 8 +/- 7 microU/min (p less than 0.01). Moreover, calcitonin gene-related peptide inhibited glucose-induced insulin secretion by 45% compared to controls (p less than 0.01), yet left terbutaline (beta 2-adrenoceptor)-stimulated insulin secretion unaffected. Furthermore, while being without effect on baseline glucagon output, calcitonin gene-related peptide potentiated terbutaline-induced glucagon secretion more than seven-fold (p less than 0.001). In contrast, the peptide did not affect baseline or stimulated pancreatic somatostatin output. We conclude that in pigs calcitonin gene-related peptide inhibits insulin secretion and potentiates glucagon secretion by direct effects on the pancreas that are not mediated by primary alterations in pancreatic somatostatin secretion. We suggest that the neuropeptide calcitonin gene-related peptide might be of importance for the intrapancreatic regulation of insulin and glucagon secretion in pigs.
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PMID:Effects of calcitonin gene-related peptide (CGRP) on islet hormone secretion in the pig. 288 86

Calcitonin is secreted by the C cells of the thyroid in response to a raised serum calcium, and acts on bone to lower serum calcium. The C cells have specific receptors for the dihydroxymetabolite of vitamin D3, 1,25(OH)2D3. Moreover, calcitonin stimulates the synthesis of 1,25(OH)2D3 in the kidney. Parathyroid hormone (PTH), the third calciotrophic hormone, is also trophic to the renal synthesis of 1,25(OH)2D3, and in turn 1,25(OH)2D3 inhibits PTH gene transcription and synthesis. We report here the marked inhibition of calcitonin gene transcription by the injection of physiologically relevant doses of 1,25(OH)2D3 to normal rats that did not raise serum calcium. Calcitonin mRNA levels after 100 pmol 1,25(OH)2D3 decreased to 6% of basal at 6 h and 4% at 48 h, and a dose response showed a marked effect even after 12.5 pmol 1,25(OH)2D3, with no appreciably greater effect with larger doses (up to 200 pmol). Control genes, actin, thyroglobulin (thyroid follicular cells), somatostatin (thyroid C-cells) were not affected by 1,25(OH)2D3. Gel blots showed that 1,25(OH)2D3 decreased calcitonin mRNA levels without any change in its size. In vitro nuclear transcription showed that 1,25(OH)2D3-treated (100 pmol) rats' calcitonin transcription was 10% of control, while thyroglobulin and actin were 100%. We propose that calcium is the major regulator of PTH and calcitonin secretion, while 1,25(OH)2D3 is an important regulator of PTH and calcitonin gene transcription. We believe this to be the first demonstration of an effect of 1,25(OH)2D3 on the C cells thereby establishing a new target organ and site of action of vitamin D. Calcitonin is trophic to 1,25(OH)2D3 synthesis, which in turn inhibits calcitonin synthesis, which are the components of a new endocrinological feedback loop.
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PMID:Regulation of calcitonin gene transcription by vitamin D metabolites in vivo in the rat. 289 28

A comparison is presented of the effect of two therapeutic doses of synthetic somatostatin (250 and 500 micrograms) and salmon calcitonin (50 and 100 U) on the blood levels of sugar, insulin (IRI), somatotropin (HGH) and cortisol in healthy volunteers following peroral administration of 75 g of glucose. Calcitonin was responsible for a significant change in glycaemia as well as IRI levels: following a retarded enhancement glycaemia as well as insulinaemia through out the first 15-30 minutes of OGTT, increased levels of both indicators were persistent at minute 120 and 180, so that the course of both curves was almost parallel. The effect was similar after SRIF had been administered, with the exception of insulin secretion being more pronounced, so that at a later stage of OGTT no hyperinsulinaemia was seen. The HGH levels tended to decrease due to both hormones, the tendency being more marked after SRIF, though statistically insignificant. There was a marked difference between the hormones as regards their effect on adrenocortical secretion. While the latter was constantly stimulated throughout OGTT under calcitonin infusion, the influence of SRIF was not significant. The metabolic and hormonal changes were found after both a lower and higher dose of both hormones, the only differences being that the inhibitory effect on the initial increase in glycaemia following a lower dose of SRIF was of no statistical significance. Hence, the metabolic and hormonal effects of calcitonin and SRIF in an acute experiment display many similarities, however, they do differ in some aspects; these effects do not depend on the doses demonstrated for both lower and higher doses of the above hormones.
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PMID:Comparison of metabolic and hormonal effects of calcitonin and somatostatin (SRIF) in the course of oral glucose tolerance test (OGTT). 289 41

Calcitonin gene-related peptide (CGRP)- and somatostatin (SRIF)-containing cells were identified by immunocytochemical techniques in pancreatic islet cells of the rat. CGRP-containing cells were found primarily in the peripheral portion of the pancreatic islets. In addition, CGRP-containing cells also contained somatostatin, which identifies the islet CGRP-containing cells as D cells. In the present study, we also tested the effect of CGRP on gastrin-releasing peptide (GRP; 10(-9) M)- or cholecystokinin (CCK-8, 10(-9) M)-stimulated release of insulin from isolated rat islets in vitro. At concentrations of 10(-8)-10(-11) M, CGRP inhibited GRP- and CCK-8-stimulated release of insulin significantly when compared with GRP or CCK-8 alone. At the lowest concentration of CGRP (10(-11) M), the inhibitory effect of CGRP on CCK-8-stimulated release of insulin was statistically significant (p less than 0.05) and exceptionally potent (65-90% inhibition). We have also found that CGRP does not stimulate the release of SRIF from isolated islet cells. These findings suggest that CGRP may play a regulatory role in the release of insulin.
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PMID:Colocalization of calcitonin gene-related peptide and somatostatin in pancreatic islet cells and inhibition of insulin secretion by calcitonin gene-related peptide in the rat. 289 52


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