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)

We evaluated the effect of seven classes of neuropeptides [bradykinin, cholecystokinin 26-33 (CCK), neurotensin, arginine-8 vasopressin (AVP), tyr-4 bombesin (BN), somatostatin, and motilin] on 18 human lung cancer and four human breast cancer cell lines to determine the pattern of responses. Flow cytometric analysis of Indo-1 AM-loaded cells was used to quantitate the intracellular calcium response of individual cells produced by these peptides alone or in simultaneous or sequential combinations. All 18 lung cancer cell lines responded to one or more peptide classes with classic small cell lines displaying the greatest responsiveness, followed by variant small-cell lines and non-small-cell lung cancer cell lines. Breast cancer cell lines demonstrated little or no response to any peptide. There was great variability in the magnitude of response and pattern of response in individual cell lines and between cell lines. Bradykinin was the most potent peptide and produced responses in the largest number of lung cancer cell lines. Simultaneous administration of active peptides produced greater intracellular calcium release than single peptides, though in a less than additive manner. Response to each peptide was followed by a refractory period lasting several hours or more. The refractoriness was peptide-specific, implying that each peptide has a distinct pathway, at least at the receptor level. Bradykinin antagonists could abrogate the calcium response to bradykinin but not to other peptides. Similarly, specific peptide antagonists for CCK, BN, and AVP blocked the response for only their specific agonist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of neuropeptides on human lung and breast cancer cells. 138 87

1. This study was designed to determine the involvement of cholecystokinin (CCK) in the gastric secretory responses to exogenous and endogenous secretagogues in conscious dogs with chronic gastric fistulae (GF), pancreatic fistulae (PF) and Heidenhain pouches (HP). 2. A meal of meat or intragastric application of peptone (300 mosM) increased secretion of HCl from the HP and pancreatic secretion of protein and plasma levels of gastrin, CCK and somatostatin. 3. The CCK receptor antagonist L-364,718 caused a further increase in the postprandial HCl secretion from the HP and in the plasma levels of gastrin and CCK but pancreatic output of protein and plasma concentration of somatostatin were significantly reduced. 4. Addition to intragastric peptone of 10% oleate or its acidification to pH 3.0 profoundly inhibited the HP secretion and gastrin release but significantly increased pancreatic secretion of protein and plasma levels of CCK and somatostatin. Administration of L-364,718 reversed the fall in the HP secretion and plasma gastrin while significantly attenuating pancreatic protein secretion and plasma somatostatin levels. 5. Intragastric administration of hyperosmolar (1200 mosM) peptone also inhibited HCl secretion from the HP but this was not affected by L-364,718. 6. Exogenous CCK and bombesin (but not gastrin) caused a small increase in HCl secretion from the HP and marked stimulation of pancreatic protein secretion accompanied by a significant rise in plasma levels of gastrin, CCK and somatostatin. Administration of L-364,718 resulted in a further increase in the HCl response of HP to bombesin and in plasma levels of gastrin and CCK but caused a reduction in plasma levels of somatostatin. 7. We conclude that CCK released by a meal of meat, intragastric peptone, oleate or acidified peptone and intravenous bombesin exerts tonic inhibitory influences on gastric acid secretion and that this effect is mediated, at least in part, by somatostatin.
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PMID:Role of cholecystokinin in the inhibition of gastric acid secretion in dogs. 140 19

Proliferative effects of hormones on the gastrointestinal mucosa are discussed according to literature data. There are presented the trophic effects of gastrin, cholecystokinin, secretin, enteroglucagon, somatostatin, growth hormone, thyroxine, peptide YY, epidermal growth factor and submaxillary growth factor.
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PMID:[The effect of hormones on the gastrointestinal mucosa]. 141 98

The increased risk of gallstone formation in acromegalics treated with the somatostatin analog octreotide has been related to an impaired gallbladder emptying. To determine the duration of these inhibitory effects, meal-stimulated gallbladder motility, plasma cholecystokinin (CCK), and pancreatic polypeptide (PP) were measured in five acromegalics treated for 6-32 months with 200-300 micrograms octreotide daily. Meal tests were performed 45 min, 8 hr and two weeks after the last 100-micrograms subcutaneous dose. Results were compared with those in normal subjects. Integrated postprandial gallbladder contraction (-125 +/- 194 cm3/120 min) and integrated PP secretion (-0.1 +/- 0.2 nmol/liter/120 min) were completely suppressed in the 45-min study, but significantly improved (P < 0.05) when measured 8 hr (1376 +/- 322 cm3/120 min and 3.0 +/- 1.0 nmol/liter/120 min) and two weeks (1437 +/- 263 cm3/120 min and 10.6 +/- 1.6 nmol/liter/120 min) after the last dose of octreotide. The integrated gallbladder contraction in acromegalics at 8 hr was comparable to that at two weeks and to that in normal subjects, but the integrated PP response at 8 hr was significantly smaller (P < 0.05 vs two weeks and vs normals). Integrated plasma CCK secretion at 45 min (0.13 +/- 0.06 nmol/liter/120 min) was not statistically significantly different from the response at 8 hr (0.15 +/- 0.02 nmol/liter/120 min) and from that in normal subjects, but it was significantly increased at two weeks after cessation of octreotide (P < 0.05 vs 45 min and 8 hr).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postprandial gallbladder motility and plasma cholecystokinin at regular time intervals after injection of octreotide in acromegalics on long-term treatment. 142 66

Most available techniques for the quantitation of enzymatic degradation of peptide hormones are time-consuming and require expensive equipment and/or novel reagents. Our aim here was to develop a rapid and sensitive assay for the measurement of degradation of cholecystokinin octapeptide (CCK-8) as well as other short, hydrophobic peptides. The proposed technique is based on our novel observation that intact CCK-8, but not its degradation product(s), binds to Lloyd reagent, a form of aluminum silicate. When radiolabeled CCK-8 was exposed to rat liver cytosol containing endogenous CCK-degrading activity, there was a time-dependent decrease in the binding of radiolabel to aluminum silicate [from 86 to 8% over 60 min at 37 degrees C]. The decrease in binding closely paralleled the extent of CCK-8 degradation over time as assessed by high-performance liquid chromatography and immunoprecipitation with specific polyclonal antibodies to CCK-8. While aluminum silicate did not efficiently bind to C-terminal and N-terminal CCK tetrapeptides, magnesium silicate bound to both tetrapeptides (> 82%), but not to their radiolabeled degradation products. Both aluminum and magnesium silicate also extensively bound (> 82%) to other peptide hormones including Met-enkephalin, somatostatin, and secretin, but did not bind their degradation products. These binding assays will be useful in studies of peptidases which degrade cholecystokinin or other small, hydrophobic peptides.
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PMID:An aluminum silicate binding assay for quantitation of degradation of cholecystokinin octapeptide and other short peptides. 145 42

Little is known about peptide-storing endocrine cells in the gut of the Nile crocodile. As in the case of other reptiles, particularly the alligator, a limited range of peptide-storing cells was found in the gut of the crocodile. They were somatostatin, glucagon, gastrin, neurotensin and pancreatic polypeptide. The topographical distribution of cells immunoreactive to somatostatin and gastrin in the gut of the crocodile is comparable to the situation in the alligator. Glucagon and neurotensin immunoreactive cells have a much wider distribution in the gastro-intestinal tract of the crocodile compared to the alligator. Cholecystokinin and bombesin cells previously reported in the small intestine of the alligator were not detected in this study. This is the first report to demonstrate pancreatic polypeptide and serotonin immunoreactivity in the gut of a crocodilian specie.
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PMID:Bioactive peptides and serotonin in the gut endocrine cells of the crocodile, Crocodylus niloticus (Laurenti 1768): an immunocytochemical study. 151 92

Previous studies showed that EGF is produced by salivary and duodenal glands and released in saliva and duodenal secretion. Using specific radioimmunoassay of EGF, this study showed that the salivary glands and duodenal mucosa contain high levels of EGF, reaching, respectively, about 38 and 4 micrograms/g of tissue weight. EGF immunoreactivity was also found in high amounts in the pancreatic tissue (20 micrograms/g) and the pancreatic juice (32 ng/mL), where the content of EGF was found to increase in response to feeding, cholecystokinin, or bombesin and to decrease after the administration of atropine and somatostatin. Studies on the binding of EGF revealed that pancreatic acinar membranes possess the specific and saturable EGF receptors with a high affinity sites with Kd of about 4.3 nM and binding capacity of about 62 fmol/mg of protein, and with low affinity sites with Kd of 21 nM and binding capacity of about 180 fmol/mg of protein. The observed high content of immunoreactive EGF in the pancreatic tissue and the presence of high and low affinity binding sites for EGF in the pancreatic acinar membranes, as well as the high EGF output in the pancreatic juice and its alterations in response to hormonal and postprandial stimulation, suggest an important role of EGF in pancreatic physiology.
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PMID:Release and binding of epidermal growth factor in the pancreas of rats. 158 56

Somatostatin and its synthetic analogue, octreotide, inhibit gallbladder emptying and cause gallstones. Whether octreotide-induced alterations in sphincter of Oddi motility contribute to this process is unknown. We, therefore, examined the effect of octreotide on fasting and protein-stimulated sphincter of Oddi motility. In 25 anesthetized prairie dogs, sphincter of Oddi motility and gallbladder pressure were monitored during the intravenous administration of octreotide, cholecystokinin (CCK) octapeptide, atropine, the intraduodenal administration of casein, and combinations of these agents. Intravenous octreotide decreased fasting sphincter of Oddi motility index both with (59 +/- 19 vs. 84 +/- 28, P less than 0.05) and without (137 +/- 31 vs. 227 +/- 42, P less than 0.05) prior cholinergic blockade with atropine. Octreotide also prevented the increases in sphincter of Oddi motility and gallbladder pressure seen with intraduodenal casein. Exogenous CCK increased sphincter of Oddi motility index and gallbladder pressure despite the simultaneous administration of octreotide alone (357 +/- 109 vs. 137 +/- 31, P less than 0.07, and 11.2 +/- 1.0 mmHg vs. 9.6 +/- 0.6 mmHg, P less than 0.05) or the combination of octreotide and atropine (317 +/- 69 vs. 59 +/- 19, P less than 0.05, and 10.1 +/- 1.6 mmHg vs. 8.5 +/- 1.4 mmHg, P less than 0.05). We conclude that both a cholinergic and an octreotide-sensitive noncholinergic pathway stimulate fasting sphincter of Oddi motility in the prairie dog.
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PMID:Effect of octreotide on sphincter of Oddi and gallbladder motility in prairie dogs. 159 Mar 99

The development of gallstones is a well recognized complication of therapy with the long-acting somatostatin analogue, octreotide in patients with acromegaly. A group of nine acromegalic patients was treated with octreotide at doses of 300-600 micrograms daily for 8 months and the changes in fasting and post-prandial cholecystokinin release, and gall bladder motor function (determined by a radiosotopic technique) were assessed at regular intervals. In addition the development of any gallstones was determined by serial ultrasonography. Fasting cholecystokinin levels showed no significant change over 6 months, whereas the post-prandial levels demonstrated a significant decrease (p less than 0.01) during therapy, yet remained significantly higher than fasting levels. Twenty-four hours after commencing therapy gall bladder ejection fraction was decreased by 57 +/- 23 per cent and gall bladder ejection rate decreased by 63 +/- 19 per cent compared to the pretreatment values, whereas after 6 months' therapy a marked reduction in gall bladder ejection fraction (greater than 35 per cent) and gall bladder ejection rate (greater than 40 per cent) persisted in only four of nine patients. Three of these four patients with persistently impaired gall bladder motor function were subsequently shown to have developed either gallstones or biliary sludge during the course of therapy. We conclude that treatment with octreotide is associated with an impaired post-prandial release of cholecystokinin in all acromegalic patients, but gallstones only develop in those patients who, in addition, have evidence of a persistently impaired gall bladder motor response to cholecystokinin.
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PMID:Assessment of gall bladder dynamics, cholecystokinin release and the development of gallstones during octreotide therapy for acromegaly. 163 Dec 61

The protochordean octapeptide cionin is structurally a hybrid of mammalian cholecystokinin (CCK) and gastrin, and thus their possible common ancestor. To determine whether cionin behaves like CCK or gastrin, we examined its effect on canine fundic somatostatin cells and on porcine and bovine gallbladder muscles. Cionin released somatostatin with a potency (ED50 0.15 nM) and efficacy (14.8% of cell content) similar to that of CCK-8 (ED50 0.12 nM, efficacy 16.7%). The efficacies but not the potencies of CCK-8 and cionin differed from those of sulfated gastrin (0.12 nM, 9.7%), nonsulfated gastrin (0.20 nM, 9.4%), and nonsulfated CCK-8 (0.30 nM, 10.4%). CCK and gastrin stimulated contractions of porcine gallbladder muscle strips in a concentration-dependent manner with no differences in efficacy but with characteristic differences in potency. CCK-8 and cionin displayed similar potencies of ED50 2.0 and 2.6 nM; both were significantly different from the ED50 of 0.4 microM for sulfated gastrin and 2.3 microM for nonsulfated gastrin. CCK radioligand binding to membrane-enriched preparations of porcine and bovine gallbladder muscularis was specific and of high affinity. The equilibrium data revealed that binding of CCK and gastrin peptides best fit a single site. CCK-8 and cionin displayed similar affinities [Kd 0.5 nM (porcine), 0.5 nM (bovine, CCK) vs. Kd 0.8 and 0.9 nM (cionin), respectively]. These differed again significantly from Kd 0.6 and 1.5 microM (sulfated gastrin) and 0.7 and 0.2 microM (nonsulfated gastrin). The results show that cionin behaves like CCK rather than gastrin in mammals.
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PMID:Cionin, a protochordean hybrid of cholecystokinin and gastrin: biological activity in mammalian systems. 164 77


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