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)

The result of alterations in the levels of CCK, in the blood and in the cerebrospinal fluid, on the functioning of the growth hormone axis has been examined in sheep. Male Coopworth sheep of about 40 kg liveweight were given various doses of CCK either intracerebroventricularly (icv) or intravenously (iv). Other similar sheep were given various doses of a CCK antagonist (loxiglumide) by the same routes. Bolus iv administration of either 35 micrograms or 200 micrograms of CCK had no effect on plasma GH levels. When given icv, however, CCK resulted in a marked (P less than 0.01) prolonged depression in plasma GH levels. The decrease in GH secretion could be partially attenuated by concurrent administration of loxiglumide, but was completely unaffected by concurrent administration of antisomatostatin serum icv. Loxiglumide alone had no effect on plasma GH levels when given at up to 200 micrograms icv, but intravenous administration of 8 mg of the CCK antagonist resulted in an increase in plasma GH concentrations (P less than 0.05). Plasma levels of somatostatin, glucose and cortisol were unaffected by both icv and iv administration of CCK. These results show that CCK can have a strong GH-inhibiting effect in the brain. Furthermore, this effect seems to be independent of hypothalamic somatostatin, suggesting another GH-inhibiting system exists.
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PMID:Neuroendocrine regulation of growth hormone secretion in sheep. IV. Central and peripheral cholecystokinin. 178 2

Mucosal cells were prepared by enzymatic digestion of porcine gastric mucosa with pronase and collagenase. The resulting cell suspension contained 10-15% parietal cells, which responded to histamine stimulation by an up to 20-fold increase in [14C]aminopyrine accumulation over control levels. Cholecystokinin-8 (CCK-8) evoked a more moderate stimulation of [14C]aminopyrine accumulation, whereas somatostatin inhibited histamine-stimulated accumulation. Parietal cells were enriched by elutriation and isopycnic centrifugation on density gradients of Percoll. A fraction with 60% parietal cells bound approximately three times more iodinated CCK-8 than a fraction containing 70% non-parietal cells. Binding of [125I]BH-CCK-8 to preparations containing 30-60% parietal cells was specifically inhibited to about 50% by 10(-9) M unlabelled CCK-8 but not by bombesin. Cell fractions containing about 30% parietal cells also bound [125I]somatostatin. Unlabelled somatostatin at 10(-9) M inhibited tracer binding by about 50%, while CCK-8 did not affect somatostatin binding to such a preparation. The results suggest the existence of specific receptors for CCK and somatostatin on porcine parietal cells exerting a regulatory influence on acid secretion.
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PMID:Binding of cholecystokinin and somatostatin to isolated porcine gastric mucosal cells and effects on aminopyrine uptake. 197 Feb 14

Somatostatin (SOM) at doses up to 1 microgram was not effective on the motility of canine and guinea pig gallbladder smooth muscle preparations in vitro. When the preparations were contracted by field electrical stimulation (0.7 ms, 40 Hz) the cholecystokinin octapeptide (CCK OP) enhanced these contractions while SOM inhibited them. These effects were accompanied, respectively, by an increase or a decrease in [3H] acetylcholine (ACh) release in the intrinsic cholinergic nerve terminals. SOM (0.5 to 2 micrograms/kg i.v.) inhibited the spontaneous and the CCK OP-activated gallbladder pressure in conscious dogs. The effect of atropine (10-50 micrograms/kg) was similar to that of SOM when injected intravenously in conscious dogs. It is suggested that the inhibitory effect of SOM on gallbladder pressure in conscious dogs is probably mediated by a decrease in ACh release by cholinergic neurons.
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PMID:Effect of somatostatin on the canine gallbladder motility. 198 Jul 26

In this paper we describe experiments that address specific issues concerning the regulation of the mouse cholecystokinin gene in brain and intestine. The mouse cholecystokinin gene was cloned and sequenced. Extensive homology among the mouse, man and rat genes was noted particularly in the three exons and the regions upstream of the RNA start site. RNAse protection assays for each of the three exons were used to demonstrate that CCK is expressed in only a subset of tissues and that the same cap site and splice choices are used in brain, intestine as well as in cerebellum, cortex, midbrain, hypothalamus and hippocampus. CCK RNA was also noted to be detectable in kidney. Thus the same gene using the same promoter is expressed in subsets of cells that differ in their biochemical, morphologic and functional characteristics. The level of expression of CCK was also monitored during mouse cortical development and the appearance of CCK RNA was compared to glutamate decarboxylase (GAD), enkephalin and somatostatin. It was noted that each of these cortical markers was first expressed at different times during cortical development. The appearance of CCK RNA during intestinal development was also measured and found to precede appearance in cortex by several days.
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PMID:Molecular cloning of the mouse CCK gene: expression in different brain regions and during cortical development. 201 97

Somatostatin is known to inhibit the postprandial release of most gastrointestinal hormones. The aim of the present study was to evaluate the effect of an analog of somatostatin, SMS 201-995 (120 ng/kg/hr), on both meal-induced and cholecystokinin octapeptide (CCK-8, 500 ng/kg/hr)-induced peptide YY (PYY) release. Six mongrel dogs with distal ileal Thiry-Vella loops were used in this study. PYY was measured in both plasma and ileal luminal effluent. SMS 201-995 did not affect interdigestive plasma or ileal luminal PYY concentrations. CCK-8 and a fat meal both stimulated PYY release into the circulation. SMS 201-995 completely inhibited the CCK-8 and fat-stimulated circulatory release of PYY. Both CCK-8 and a mixed meal increased ileal luminal PYY recovery. SMS 201-995 inhibited CCK-8-induced, but not meal-induced, ileal luminal PYY recovery. These findings support previous studies that describe independent circulatory and ileal luminal PYY release. We conclude that both somatostatin and CCK may have a regulatory role in postprandial circulatory release of PYY.
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PMID:The effect of SMS 201-995 on meal and CCK-stimulated peptide YY release. 203 80

Intracerebroventricular administration of SMS 201-995 (5 micrograms/rat), a somatostatin analogue, induced barrel rotation in rats. Pretreatment with ceruletide (40 micrograms/100 g b. wt., IP) 3 days or 7 days prior to the injection of SMS 201-995 significantly inhibited the response rate of barrel rotation induced by SMS 201-995, but not that induced by arginine-vasopressin (1 microgram/rat, ICV). The suppressive effect of ceruletide on barrel rotation could be partially countered by MK-329, a selective peripheral CCK (CCK-A) receptor antagonist. Desulfated cerulein did not affect the barrel rotation induced by SMS 201-995. These findings suggest that ceruletide specifically suppresses the barrel rotation evoked by SMS 201-995 in a long-lasting manner possibly acting through CCK-A receptor.
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PMID:Barrel rotation in rats induced by SMS 201-995: suppression by ceruletide. 208 92

The central action of peptides to influence GI motility in experimental animals is summarized in Table 1. TRH stimulates gastric, intestinal, and colonic contractility in rats and in several experimental species. A number of peptides including calcitonin, CGRP, neurotensin, NPY, and mu opioid peptides act centrally to induce a fasted MMC pattern of intestinal motility in fed animals while GRF and substance P shorten its duration. The dorsal vagal complex is site of action for TRH-, bombesin-, and somatostatin-induced stimulation of gastric contractility, and for CCK-, oxytocin- and substance P-induced decrease in gastric contractions or intraluminal pressure. The mechanisms through which TRH, bombesin, calcitonin, neurotensin, CCK, and oxytocin alter GI motility are vagally mediated. An involvement of central peptidergic neurons in the regulation of gut motility has recently been demonstrated in Aplysia, indicating that such regulatory mechanisms are important in the phylogenesis. Alterations of the pattern of GI motor activity are associated with functional changes in transit. TRH is so far the only centrally acting peptide stimulating simultaneously gastric, intestinal, and colonic transit in various animals species. Opioid peptides acting on mu receptor subtypes in the brain exert the opposite effect and inhibit concomitantly gastric, intestinal, and colonic transit. Bombesin and CRF were found to act centrally to inhibit gastric and intestinal transit and to stimulate colonic transit in the rat. The antitransit effect of calcitonin and CGRP is limited to the stomach and small intestine. The delay in GI transit is associated with reduced GI contractility for most of the peptides except central bombesin that increases GI motility. Nothing is known about brain sites through which these peptides act to alter gastric emptying and colonic transit. Regarding brain sites influencing intestinal transit, TRH-induced stimulation of intestinal transit in the rat is localized in the lateral and medial hypothalamus and medial septum. The periaqueductal gray matter is a responsive site for mu receptor agonist- and neurotensin-induced inhibition of intestinal transit. The neural pathways from the brain to the gut whereby these peptides express their stimulatory or inhibitory effects on GI transit is vagal dependent with the exception of calcitonin. It is not known whether the vagally mediated inhibition of GI transit by these peptides results from a decrease activity of vagal preganglionic fibers synapsing with excitatory myenteric neurons or an activation of vagal preganglionic neurons synapsing with inhibitory myenteric neurons. The lack of specific antagonists for these peptides has hampered the assessment of their physiological role.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Central nervous system action of peptides to influence gastrointestinal motor function. 210 14

The proximal duodenum of eight marsupial species, (koala, common brushtail possum, ring-tailed possum, common wombat, great grey kangaroo, parma wallaby, short-nosed bandicoot and tiger cat) were investigated immunohistochemically using 12 specific antisera for gut hormones. Several types of immunoreactive cells were seen on the intestinal villi and in crypts of these species: 9 types in the koala; 8 types in the common brushtail possum; 7 types in the common wombat; 6 types in the short-nosed bandicoot and 5 types in the ringtailed possum, great grey kangaroo, parma wallaby and tiger cat. Gastrin-, somatostatin-, motilin- and serotonin-immunoreactive cells were seen in all species examined. A few BPP-, enteroglucagon-, CCK-, secretin-, GIP- and neurotensin-immunoreactive cells were seen but only in few species. A few substance P-immunoreactive cells were detected only in the koala. Immunoreactive cells were also seen in Brunner's glands: 5 types in the parma wallaby; 3 types in the great grey kangaroo and tiger cat; 2 types in the koala and common wombat; 1 type in the short-nosed bandicoot. No immunoreactive cells were found in Brunner's glands of the common brushtail possum.
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PMID:An immunohistochemical study of endocrine cells in the proximal duodenum of eight marsupial species. 218 87

We report a case of multiple duodenal ulcers with gastric hypersecretion due to a nongastrin secretagogue produced by a malignant tumor of the pancreas in a 78-year-old man. The case resembled a Zollinger-Ellison syndrome (ZES) with high acid output (basal acid output 27, sham meal-stimulated 37, maximum acid output 47 mEq/h), but with fasting gastrin 43 pg/ml, nonresponsive to secretin. As in ZES, pepsin output was comparatively low, and secretion was inhibitable by atropine (50% inhibited by 1 microM). The tumor removed at surgery contained less than 1 ng gastrin per gram, but was many times more potent than pentagastrin in stimulating acid from a lumen-perfused rat stomach. The tumor also contained cholecystokinin (CCK-8 and CCK-33), motilin, insulin, and somatostatin, which were also present in adjacent normal pancreas; in addition, the tumor contained pancreatic polypeptide and pancreatic cancer-associated antigen. This case represents a rare syndrome due to an as yet undefined peptide secreted by a (frequently malignant) pancreatic endocrine tumor and masquerading as ZES. This is the first report of studies of pepsin secretion and of the effect of atropine, suggesting that the physiologic effects of the secretagogue resemble that of gastrin.
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PMID:A nongastrin malignant ampullary tumor causing gastric acid and pepsin hypersecretion. A case report. 223 2

Using the avidin-biotin-peroxide immunohistochemical method, we studied the distributions of somatostatin (SOM)-, cholecystokinin-8 (CCK-8)- and substance P (SP)-like immunoreactivities in the cerebellum of macaque monkeys at embryonic day 120 (E120), E140, newborn, postnatal day 60 (P60) and adults. During the embryonic stages, there were many SOM-, CCK- and SP-immunoreactive structures in the external granular layer, Purkinje cell layer and white matter, SP-immunoreactive mossy fibers and their terminals were distributed in the granular layer and white matter. During these stages, there were SOM-immunoreactive Purkinje cells, Golgi cells and a few cells in the molecular layer, and CCK-immunoreactive Purkinje cells and cells in the molecular layer. At the newborn stage, all of the immunoreactivities in the external granular layer decreased and the number of immunoreactive fibers increased in the white matter. At P60 stage, SOM- and CCK-immunoreactive fibers were observed around Purkinje cells, which seem to be the fiber terminals of basket cells. Many SOM, CCK and SP fibers were distributed in the white matter. In the adult stage, we observed little neuropeptide-immunoreactivity in the cerebellum. The high concentration of the neuropeptide-immunoreactive fibers and cells in the earlier stages suggests that the neuropeptides may be involved in the development of the primate cerebellar cortex.
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PMID:Neuropeptide-immunoreactive cells and fibers in the developing primate cerebellum. 229 93


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