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)

In light of the effects of gastrointestinal (GI) peptides on bile secretion and biliary tract mobility, we studied the effects of GI peptides on gallstone formation in guinea pigs fed on low protein lithogenic diet. The peptides under study included cholecystokinin octapeptide (CCK-8), vasoactive intestinal peptide (VIP), somatostatin (SRIF), secretin (SEC), and neurotensin (NT). Hepatic bile flow, electrolytes, and other bile components were also measured. It was found that CCK-8 and VIP suppressed the formation of gallstones and increased hepatic bile flow and Na+, K+, Cl- output significantly. On the other hand, SRIF significantly promoted gallstone formation. The rates of gallstone formation in CCK-8, VIP, and SRIF treated guinea pigs were 15.4%, 23.5%, and 88.0%, respectively, in contrast to 56.8% in the control group. The inhibitory effect of CCK-8 and promoting effect of SRIF on gallstone formation were dose-dependent.
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PMID:Effects of gastrointestinal peptides on formation of gallstone in guinea pigs. 167 24

The effect of synthetic rat amylin (10,100,1000 pmol/l) on glucose (10 mmol/) and arginine (10 mmol/l) -stimulated islet hormone release from the isolated perfused rat pancreas and on amylase release from isolated pancreatic acini was investigated. Amylin stimulated the insulin release during the first (+76%) and the second secretion period (+42%) at 1 nmol/l. The first phase of the glucagon release was inhibited concentration dependently by amylin and completely suppressed during the second phase. Amylin diminished the somatostatin release in a concentration dependent manner. This effect was more pronounced at the first than the second secretion period (1 nmol amylin: 1 phase: -60%, 2.phase: -22%). Amylin was without any effect on basal and CCK stimulated amylase release from isolated rat pancreatic acini. Our data suggest amylin, a secretory product of pancreatic B-cells, as a peptide with approximately strong paracrine effects within the Langerhans islet. Therefore, amylin might be involved in the regulation of glucose homeostasis.
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PMID:Islet amyloid polypeptide (IAPP;amylin) influences the endocrine but not the exocrine rat pancreas. 169 Sep 93

The effects of bombesin on the growth of the gastroduodenal mucosa and the pancreas have been examined in adult rats with intact or resected antrum and following administration of somatostatin or CCK-receptor antagonist L-364,718. The peptides were administered three times daily for 7 consecutive days, and then the animals were sacrificed and growth parameters (organ weight and RNA and DNA contents) were determined, and plasma gastrin and CCK were assayed. Compared with the control (saline) values, bombesin significantly stimulated the growth of the oxyntic and duodenal mucosa and the pancreas. These effects were partly reduced but not abolished by somatostatin, antrectomy and L-364,718, suggesting that bombesin may enhance the growth partly by releasing gastrin and CCK and partly by direct action on these tissues.
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PMID:Role of gastrin and cholecystokinin in the growth-promoting action of bombesin on the gastroduodenal mucosa and the pancreas. 169 18

An immunocytochemical investigation was carried out on round and spreading hemocytes of Planorbarius corneus by using 20 antisera to vertebrate bioactive peptides. The immunotests showed the presence of alpha 1-antichymotrypsin-bombesin-, calcitonin-, CCK-8 (INC)-, CCK-39-, gastrin-, glucagon-, Met-enkephalin-, neurotensin-, oxytocin-, somatostatin-, substance P-, VIP-, and vasopressin-immunoreactive molecules in the spreading hemocytes. The round hemocytes were only positive to anti-bombesin, anticalcitonin, anti-CCK-8 (INC), anti-CCK-39, anti-neurotensin, anti-oxytocin, anti-substance P and anti-vasopressin antibodies. No immunostaining was observed with anti-CCK-8 (Peninsula), anti-insulin, anti-prolactin, anti-thyroglobulin and anti-thyroxin (T4) antibodies. As probably in vertebrates, these bioactive peptides may modulate immuno cell function.
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PMID:Immunocytochemical evidence of vertebrate bioactive peptide-like molecules in the immuno cell types of the freshwater snail Planorbarius corneus (L.) (Gastropoda, Pulmonata). 169 11

The effects of two recently isolated mammalian FMRFamide related peptides (A-18-F-amide and F-8-F-amide) on the encocrine and exocrine rat pancreas were investigated. A-18-F-amide (10, 100, 1000 pM) inhibited concentration dependently glucose (10 mM)- and arginine (10 mM)-induced insulin secretion from the isolated perfused rat pancreas during the first (controls: 100%; 10 pM: 114%; 100 pM: 63%, p less than 0.05; 1000 pM: 31%, p less than 0.05) and the second secretion phase (controls: 100%; 10 pM: 102%; 100 pM: 78%; 1000 pM: 27%, p less than 0.05). The inhibitory actions of A-18-F-amide on pancreatic D-cell secretion were more pronounced during the first than the second phase (first phase: controls: 100%; 10 pM: 95%; 100 pM: 37%, p less than 0.05; 1000 pM: 39%, p less than 0.05%; second phase: controls: 100%; 10 pM: 113%; 100 pM: 72%; 1000 pM: 59%, p less than 0.05). F-8-F-amide (at 1000 pM) inhibited stimulated insulin (controls: 100%; first phase: 26%, p less than 0.05%; second phase: 20%, p less than 0.05) and somatostatin release (controls: 100%; first phase: 14%, p less than 0.05; second phase: 29%, p less than 0.05). Both peptides were without effect on basal and CCK-8-stimulated amylase release from isolated incubated rat pancreatic acini.
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PMID:The effects of two FMRFamide related peptides (A-18-F-amide and F-8-F-amide; 'morphine modulating peptides') on the endocrine and exocrine rat pancreas. 170 9

The axonal transport blocker colchicine has been extensively used in immunohistochemical studies to induce accumulation of neuroactive compounds, especially neuropeptides, in neuronal somata and thus improve their visualization. To assess whether colchicine might, in addition, influence the synthesis of such compounds, we have now used in situ hybridization to examine the levels of mRNAs encoding for several neuropeptides (galanin [GAL], cholecystokinin [CCK], somatostatin [SOM], neuropeptide Y [NPY]) and neurotransmitter-synthesizing enzymes (choline acetyltransferase [ChAT], tyrosine hydroxylase [TH], amino acid decarboxylase [AADC], and glutamic acid decarboxylase [GAD]) after intraventricular administration of the drug. The results show that colchicine differentially modifies the levels of several mRNA species in different brain areas. Thus GAL mRNA levels increase in virtually all regions examined, including the basal forebrain, hypothalamus, dorsal raphe nucleus, locus coeruleus, and nucleus tractus solitarii. In addition, after colchicine treatment, GAL mRNA appears to be induced in the ipsilateral hemisphere in regions such as the cortex, hippocampus, striatum, lateral septum, and some nuclei of the thalamus as well as within white matter, where it cannot be detected in control animals. Although GAL mRNA in the vast majority of cases is neuronal, some findings indicate a possible glial localization. In parallel, colchicine depletes ChAT mRNA and increases GAD mRNA in the basal forebrain and striatum and decreases AADC mRNA in the dorsal raphe nucleus and locus coeruleus. In the latter nucleus, NPY and TH mRNA levels are increased by colchicine. In contrast, TH mRNA and also CCK mRNA levels decrease in the substantia nigra. In the cortex, hippocampus, and thalamus ipsilateral to colchicine injection CCK mRNA levels are markedly decreased, whereas SOM mRNA is decreased and NPY mRNA increased in the hippocampus but unchanged in the cortex. The results are discussed with reference to the possible artifacts that the use of colchicine might induce in immunohistochemical mapping studies and in relation to possible neurotoxic actions of colchicine, in some cases perhaps related to impaired retrograde transport of growth factor(s).
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PMID:Differential effects of intracerebroventricular colchicine administration on the expression of mRNAs for neuropeptides and neurotransmitter enzymes, with special emphasis on galanin: an in situ hybridization study. 170 58

This work investigates the effects of the long-acting somatostatin analogue, octreotide also named SMS 201-995 or Sandostatin, on pancreatic growth in function of the dose and duration of treatment. Octreotide was administered s.c. twice daily, while pancreatico-trophic peptides, caerulein and CCK-8 (1.8 nmol/kg b.wt.) or GRP (3.6 nmol/kg b.wt.) were administered s.c. three times daily. Octreotide (1,10,20 micrograms/kg b.wt.) administered for 4 days reduced pancreatic growth induced by caerulein in a dose-dependent manner. This effect, significant from 10 micrograms/kg, was more obvious with 20 micrograms/kg. At this latter dose, octreotide inhibited significantly the increase in pancreatic weight and protein, RNA, DNA and enzyme content induced by a 4- or 10-day treatment with GRP. A similar effect was observed after a 4-day treatment with CCK-8, but after a 10-day treatment only protein and enzyme contents were reduced. Octreotide by itself did not affect pancreatic size and composition after a 10-day treatment, but decreased enzyme content after a 4-day treatment. It is concluded that octreotide exerts an antitrophic effect on the rat exocrine pancreas which depends on the dose and duration of treatment and can be modulated by the trophic factor applied for a long-term.
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PMID:Effect of prolonged administration of long-acting somatostatin on caerulein, CCK-8 and GRP induced pancreatic growth in the rat. 170 49

In the preceding paper, by means of selective agonists to gastrin (HG-17) and cholecystokinin (CCK-39), we evidenced the existence of "gastrin-type" receptors that could regulate histamine release and "CCK-type" receptors that could stimulate somatostatin release in isolated rabbit fundic non-parietal cells (F1 cells). Furthermore, these receptors could induce phosphoinositide breakdown. To confirm the involvement of these receptor types in these biological and biochemical processes, we used selective antagonists, L-364,718 (3-(benzoylamino)-benzodiazepine) specific to "CCK-A-type" receptor and L-365,260 (3-(acylamino)-benzodiazepine) specific to "gastrin/CCK-B-type" receptor. Neither L-364,718 nor L-365,260 alone caused any significant stimulation of [3H]inositol phosphate ([3H]InsP) production and release of histamine or somatostatin-like immunoreactivity (SLI). Each analogue inhibited in a dose-dependent manner [125I]HG-17 or [125I]CCK-39 binding to F1 cells, [3H]InsP accumulation and histamine and SLI release stimulated by HG-17 or CCK-39. L-365,260 appeared to be 30-70 times more potent than L-364,718 in inhibiting [125I]HG-17 binding to F1 cells, as well as HG-17-induced [3H]InsP accumulation and HG-17-or CCK-39-enhanced histamine release (IC50 values: approximately 5-20 nM for L-365,260 and approximately 200-1500 nM for L-364,718). In contrast, L-364,718 was 200 to 400 times more potent than L-365,260 in inhibiting [125I]CCK-39 binding to F1 cells, CCK-39-induced [3H]-InsP accumulation and SLI release stimulated by CCK-39 or HG-17 (IC50 values: approximately 0.3-1 nM for L-364,718 and 100-200 nM for L-365,260). These results led to conclude: (i) the existence of a "gastrin-type" receptor related to histamine release: (ii) the existence of a "CCK-A-type" receptor related to somatostatin release; (iii) the existence of "gastrin type" and "CCK-A-type" receptors linked to the phosphoinositide breakdown pathway.
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PMID:"Gastrin" and "CCK" receptors on histamine- and somatostatin-containing cells from rabbit fundic mucosa-II. Characterization by means of selective antagonists (L-364,718 and L-365,260). 171 76

Neuropeptide Y (NPY) is a unique 36 amino acid peptide with strong sequence homology to pancreatic polypeptide and peptide YY. In the rat pancreas, NPY-positive fibers have been demonstrated in close association with exocrine structures, suggesting a regulatory role for the peptide. In conscious rats with pancreatic ductal cannulas, amylase output stimulated by cholecystokinin octapeptide (CCK-8: 0.2 microgram kg - 1 h -1) was dose-dependently inhibited by intravenous NPY infusion (20, 40, and 80 micrograms kg-1 h-1). Inhibitory effects were rapid in onset but reversed with cessation of NPY infusion. With continuous NPY infusion (40 microgram kg-1 h-1), prolonged inhibition of amylase output by the vagal stimulant 2-deoxyglucose (100 mg kg-1) was observed (greater than 50% inhibition in each of none consecutive 10-min periods). In contrast, NPY infusion in doses of 20, 40, or 80 micrograms kg-1 h-1 produced no alteration in immunoreactive somatostatin levels. In vitro, NPY incubation (10(-13)-10(-8) M) produced no change in basal amylase release from dispersed, purified acinar cells. In addition, co-incubation of NPY (10(-8)-10(-6) M) with CCK-8 (10(-13)-10(-8) M) produced no inhibition of CCK-stimulated amylase release from dispersed acini. In contrast, NPY (10(-6) M) produced significant inhibition of amylase release from pancreatic lobules that had been stimulated by 75 mM potassium (135 +/- 11% versus 177 +/- 18% of basal level) or by 25 microM veratridine (196 +/- 19% versus 398 +/- 152%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of rat pancreatic exocrine secretion by neuropeptide Y: studies in vivo and in vitro. 171 87

The ability of somatostatin analogs to interact with the binding of cholecystokinin has been studied in pancreatic and brain cortical membranes. Only the 28 amino-acid forms of somatostatin (S28), [Nle8]S28 and [Des Lys14,DTrp22]S28 were found to inhibit the binding of cholecystokinin to rat pancreatic plasma membranes and to increase the amylase release from pancreatic acini. This effect was independent of somatostatin receptor and resulted from an interaction between S28 and CCK receptor. This interaction was not observed with [Leu8, DTrp22, Tyr25]S28, indicating that this analog does not possess the biological activity of the native peptide and that the iodinated peptide could not label specific S28 receptors. S28 interacted also with CCK receptors in cortical brain membranes. Our results support the concept that S28, but not S14, may function as a regulatory molecule at CCK receptors and emphasize that S28 and S14 may be distinct neuromodulators.
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PMID:Somatostatin 28 interacts with CCK receptor in brain and pancreas. 171 46


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