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)

A disturbed intraduodenal milieu and pancreatic scarring in advanced chronic pancreatitis (CP) may lead to changes of gut and pancreatic hormones. In the present study, the gastroduodenal mucosal content of several regulatory peptides was determined in 8 patients with severe calcific CP and 8 healthy volunteers. In addition, hormone release into the bloodstream was estimated after intraduodenal acid/glucose stimulation in the control subjects and 8 CP patients each with or without secondary diabetes mellitus (DM), and in 8 patients with juvenile DM, so that disturbed gut hormone release could be attributed either to CP or DM. While VIP release into the circulation was similar in all participants, mucosal levels of VIP and substance P were significantly elevated in the duodenal bulb and descending duodenum of CP patients. The somatostatin content of gastroduodenal mucosa in CP was at least as high as in normals. Gastrin was significantly more abundant only in the duodenal bulb of CP patients, while plasma gastrin was normal. Duodenal CCK concentrations tended to be elevated in the duodenal bulb, but not significantly. The release of secretin seemed to be higher in type-1 diabetics than in CP patients. The mucosal pattern of GIP was nearly identical in CP patients and controls. Compatible with this finding, the GIP release did not show any peculiarities in CP with or without DM or in DM. Basal and stimulated plasma levels of motilin were abnormally high in CP. Pancreatic polypeptide plasma levels were normal in DM, but significantly reduced in CP, especially in CP with DM. Fasting PP and stimulated pancreatic enzyme outputs were linearly related.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic pancreatitis and diabetes mellitus: plasma and gastroduodenal mucosal profiles of regulatory peptides (gastrin, motilin, secretin, cholecystokinin, gastric inhibitory polypeptide, somatostatin, VIP, substance P, pancreatic polypeptide, glucagon, enteroglucagon, neurotensin). 246 85

The authors report the time of appearance, morphology and topographic distribution of gastrin/cholecystochinin- (G/CCK-), somatostatin- (SRIF-), neurotensin- (NT-), motilin- (MO-) and substance P-like immunoreactive (SP-LI) elements during embryonic and postnatal development, in ileum, caeca and colon of chick embryos (from 8 days of incubation to hatching), newborn chicks (up to 15-days old) and adult chickens. In the ileum, G/CCK-LI and SP-LI cells appeared on day 11, the others on about day 13. In the caeca the first cells of all types were seen from about day 17. In the colon, NT-LI cells appeared early, on day 9, SP-LI and occasional SRIF-LI cells from day 13 on and MO-LI and G/CCK-LI only from day 17. In the ileum all the cells studied were present, in the caeca and colon they were extremely scarce, apart from NT-LI cells which were more numerous. In the prenatal stages, SP-LI was found only in epithelial cells; after hatching, it was also present in metasympathetic nerve elements.
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PMID:Ontogenesis of endocrine cells in the chicken intestine: an immunohistochemical study. 246 15

The interaction of insulin and somatostatin on amylase secretion was examined in the isolated perfused rat pancreas. Exogenous insulin (10 mU/ml) significantly potentiated cholecystokinin- (CCK; 0.5 mU/ml) stimulated amylase secretion (12.47 +/- 2.9 micrograms/ml, n = 7). Glucose (16.7 mM) stimulated endogenous insulin secretion (523 +/- 66 microU/ml) and also significantly enhanced CCK-stimulated amylase secretion (13.41 +/- 2.8 micrograms/ml, n = 11). When somatostatin was included in the perfusion media, containing insulin and CCK, amylase secretion was reduced to 3.17 +/- 0.83 micrograms/ml (n = 7), a level comparable to that of CCK-stimulated amylase secretion alone. Similarly, addition of exogenous somatostatin to perfusion media, containing 16.7 mM glucose and CCK, reduced amylase secretion to 4.29 +/- 1.09 micrograms/ml (n = 9). The effect of somatostatin and insulin on carbamylcholine-stimulated amylase secretion was also examined. Exogenous insulin (50 mU/ml) potentiated carbamylcholine- (10(-8) M) stimulated amylase secretion, and addition of exogenous somatostatin to the media containing both insulin and carbamylcholine suppressed the insulin potentiation. Uptake of 125I-[Tyr11]somatostatin in the perfused pancreas was saturable as it decreased significantly with the addition of excess unlabeled somatostatin. Autoradiograms revealed uptake of the ligand by both the endocrine islets and the exocrine pancreas with the highest density of grains observed over the acini. These results support the hypothesis that islet peptides modulate the exocrine pancreas, that somatostatin inhibits amylase secretion by inhibiting the action of insulin, and that somatostatin may act directly on the exocrine pancreas via specific receptors on acinar cells.
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PMID:Effects of islet hormones on amylase secretion and localization of somatostatin binding sites. 247 Feb 60

At present our knowledge of enteric peptide-containing neurons in man is limited. In this study we have used human appendices removed at surgery to examine the peptidergic innervation by immunocytochemistry, immunochemistry, and pharmacological in vitro experiments. Immunocytochemistry revealed a variety of peptide-containing nerve fiber populations in the human appendix. VIP/PHI-, VIP/PHI/NPY-, SP/NKA-, galanin-, and enkephalin-containing nerve fibers were numerous; CGRP- and GRP-containing nerve fibers were moderate in number, while only scattered NPY-, enkephalin/BAM-, and somatostatin-containing nerve fibers could be found. No CCK-, dynorphin A-, or dynorphin B-immunoreactive nerve fibers could be detected. The coexistence of VIP/PHI, SP/NKA, and enkaphalin/BAM can be anticipated from the known sequence of their respective precursors. However, the coexistence of VIP/PHI and NPY was unexpected but corroborates previous observations in other species. Interestingly, SP and CGRP did not seem to coexist in nerve fibers of the human appendix. Immunochemistry (RIA and HPLC) confirmed the presence of VIP, NPY, SP, galanin, CGRP, GRP, enkephalin, and somatostatin. Motor activity studies suggest that acetylcholine plays a major role in the electrically evoked contractions, since atropine suppressed these contractions. Galanin (10(-8)-10(-6) M) and GRP (10(-9)-10(-7) M) caused concentration-dependent contractions that were unaffected by tetrodotoxin and thus probably reflect a direct action on smooth muscle receptors. GRP (10(-9) M) enhanced the electrically induced cholinergic contraction (to 193 +/- 24%), while met-enkephalin (10(-6) M) reduced it (to 54 +/- 6%). Both peptides failed to affect the contractile response to exogenous acetylcholine and probably act to modulate the release of acetylcholine. NPY, VIP, CGRP, SP, and somatostatin failed to induce contraction or to affect the electrically evoked contractions.
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PMID:Neuropeptides in the human appendix. Distribution and motor effects. 247 67

In this study we examine the mechanism by which somatostatin (SRIF-14) inhibits cholecystokinin octapeptide- (CCK-8) but not substance P-mediated release of [3H]acetylcholine (ACh) from the guinea pig ileum. 2',5'-Dideoxyadenosine, an inhibitor of adenylate cyclase, antagonized the action of CCK-8 and forskolin but had no effect on substance-P-evoked release of [3H]ACh. Addition of theophylline enhanced the release of [3H]ACh stimulated by CCK-8 but not by substance P. These observations suggest that CCK-8, but not substance P, can stimulate cholinergic transmission via an adenosine 3',5'-cyclic monophosphate (cAMP)-dependent pathway. Somatostatin inhibited release of [3H]ACh evoked by CCK-8 and forskolin in a dose-related manner. CCK-8- and forskolin- but not substance P-evoked release of [3H]ACh were maximally inhibited in the presence of 10(-6) M somatostatin (49 +/- 5 and 48 +/- 7% of control, respectively). Pretreatment with pertussis toxin (inactivates inhibitory guanine nucleotide binding proteins) reversed the inhibitory effect of somatostatin on the release of [3H]ACh evoked by CCK-8. These observations suggest that CCK-8 but not substance P can stimulate [3H]ACh by a cAMP-dependent pathway. Somatostatin appears to inhibit the cAMP-dependent component of CCK-8-mediated cholinergic transmission via activation of a pertussis toxin-sensitive G protein.
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PMID:Differential action of somatostatin on peptide-induced release of acetylcholine. 247 31

Authors investigated the inhibitory effect of somatostatin on pancreatic enzyme secretion in vivo and in vitro, in rats. In conscious animals somatostatin strongly inhibited pancreatic amylase secretion. In vitro, however, amylase secretion was not affected by the peptide: it had no affect either on basal secretion, or on stimulated secretion induced via CCK-, or cholinergic receptors. Furthermore, it did not modify nerve-stimulation induced enzyme secretion. The results suggest that the in vivo inhibitory action somatostatin on pancreatic enzyme secretion is an indirect one.
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PMID:[The effect of somatostatin on pancreatic enzyme secretion in rats in vivo and in vitro]. 247 42

This paper was addressed to know whether early events in mitogenesis (activation of the Na+/H+, activation of ornithine decarboxylase and formation of cyclic AMP) are involved in pancreatic cell proliferation and mediate secretory process. The AR4-2J cell line was used. Analogues of amiloride inhibited cell proliferation but had no effect on amylase release. Activation of ornithine decarboxylase was triggered via a CCK B receptor type not involved in pancreatic secretion. Inhibition of cyclic AMP was not involved in inhibition of cell proliferation caused by somatostatin. Specific effectors might be related either to the secretory or to the trophic pathway. Another possibility is that multiple receptor sub-classes are linked to specific pathways.
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PMID:Interrelation of secretory and trophic responses in the exocrine pancreas. 248 97

Intraperitoneal injection of 5 micrograms cholecystokinin octapeptide (CCK-8) into male rats deprived of food for 48 h produced a transient (less than 15 min) increase in plasma levels of CCK-8 but suppressed food intake for an extended period (45 min). Plasma concentrations of CCK-8 after i.p. injection of CCK-8 were raised to levels which were fairly comparable to those after feeding. Intracerebroventricular (i.c.v.) injection of the CCK antagonist proglumide (100 micrograms) reversed the effect of CCK-8 on food intake, while i.p. injection of proglumide (100 micrograms) did not have this effect. Feeding increased the plasma concentrations of somatostatin and gastrin but not of oxytocin, and somatostatin and oxytocin but not gastrin were released in response to i.p. injection of CCK-8. However, neither somatostatin nor oxytocin affected food intake, and their release in response to CCK-8 was unaffected by i.c.v. injection of proglumide. These results support the suggestion that CCK-8 is a physiological 'satiety' peptide, which can affect food intake in rats by mechanisms involving both peripheral and central CCK receptors.
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PMID:Plasma concentrations of cholecystokinin octapeptide and food intake in male rats treated with cholecystokinin octapeptide. 256 47

Parafollicular C cells of the rat thyroid contain several immunoreactive peptides including calcitonin (CT), calcitonin gene-related peptide (CGRP), somatostatin and a C-terminal gastrin/CCK immunoreactive epitope as shown at the light- and electron-microscopical levels. Adult thyroid C cells are strongly immunoreactive to CT and most of the cells also react strongly with CGRP antisera and weakly with a gastrin/CCK antiserum. The latter antiserum may cross-react with CGRP. This cross-reactivity probably only occurs at very high concentrations of CGRP observed in adult thyroid C cells, but not in intrathyroidal CGRP-containing nerves, nor in early neonatal C cells. In neonatal rats, somatostatin immunoreactive C cells are numerous and most of these cells are also CT and CGRP immunoreactive. In contrast, only few C cells display somatostatin immunoreactivity in adult rat thyroids. Sequential staining experiments revealed that some thyroidal C cells simultaneously express all four types of immunoreactivity. At the electron microscopical level, all of these immunoreactivities were observed in secretory granules of C cells. Double- and triple-staining experiments, moreover, documented that some peptides are co-localized in the same granules.
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PMID:Light- and electron-microscopical localization of calcitonin, calcitonin gene-related peptide, somatostatin and C-terminal gastrin/cholecystokinin immunoreactivities in rat thyroid. 256 89

The aim of this study was to localize the high-affinity uptake of [3H]-GABA in Langerhans islets of rats aged 2.5, 7.5, and 75 days. On high-resolution autoradiography, cells presenting characteristic somatostatin granules were labeled, whereas others containing similar granules appeared nearly devoid of silver grains. Immunogold detection with antisomatostatin antibodies and high-resolution autoradiography suggested that uptake of GABA is indeed performed by somatostatin cells. To test the heterogeneity of uptake frequency in somatostatin cells, a second approach, coupling immunohistochemistry with anti-somatostatin, anti-PP, anti-glucagon, anti-glicentin, and anti-CCK antibodies, and low-resolution autoradiography, was applied on paraffin sections. It demonstrated that the uptake ability is not characteristic of all the somatostatin cells but of only a subpopulation of them. A few cells not immunoreactive to the anti-somatostatin antiserum also appeared to be able to take up GABA. Moreover, except for a rare few, the PP-glucagon-, glicentin-, and CCK-39-immunoreactive cells were not labeled by autoradiography.
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PMID:High-affinity GABA uptake in a subpopulation of somatostatin cells in rat pancreas. 256


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