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)

Several commercial insulin preparations were found to contain significant quantities of pancreatic glucagon, pancreatic polypeptide (P.P.), vasoactive intestinal peptide (V.I.P.), and somatostatin, though these substances were effectively absent from the new highly purified or monocomponent insulins. Of 448 insulin-dependent diabetics receiving conventional insulins, 63% had circulating antibodies to human P.P., 6% antibodies to V.I.P., 6% to glucagon, and 0.5% to somatostatin. The antibodies were of high affinity and were commonest in the younger diabetics. No antibodies were detected in 167 maturity-onset diabetics, in 125 healthy controls, or in 22 patients treated only with monocomponent insulin. Immunocytochemical testing showed that antibody-positive diabetic plasma reacted specifically against the corresponding hormone-producing pancreatic endocrine cells, against enteroglucagon and somatostatin cells outside the pancreas, and against V.I.P.-containing autonomic nerves throughout the body. The finding of iatrogenic autoimmunity and naturally occurring hormones in large numbers of insulin-dependent diabetics raises important questions about long-term treatment.
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PMID:Autoimmunity in diabetics induced by hormonal contaminants of insulin. 8 63

Porcine vasoactive intestinal peptide stimulated adenosine 3':5'-monophosphate (cyclic AMP) production in rat intestinal epithelial cells. The stimulation was dependent on time and temperature and was potentiated by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. Under optimal conditions (at 15 degrees C, with 0.2 mM 3-isobutyl-1-methylaxanthine, at a cell concentration up to 18 microgram DNA/ml), the cyclic AMP production produced by vasoactive intestinal peptide was constant for 10 min and stopped after 15 min incubation, at either low (1 nM) or high (30 nM) concentration of the peptide. This plateau effect was demonstrated not to be due to an inactivation of vasoactive intestinal peptide in the medium nor to an alteration of receptors for the peptide. Cyclic AMP production was sensitive to a concentration as low as 0.1 nM vasoactive intestinal peptide. Maximal stimulation of cyclic AMP levels by vasoactive intestinal peptide was observed with 30 nM vasoactive intestinal peptide and represented an 11-fold increased above basal. The dorse-response curve was monophasic with a Km of 2.3 x 10(-9) M. No cooperative effects were detected by Hill analysis. The positive non-linear relationship observed between stimulation of cyclic AMP production and occupancy of binding site was not time-dependent as indicated by experiments performed after 15, 45 and 120 min incubation. Maximal and half-maximal responses were obtained at about 70% and 7% occupation of binding sites, respectively. Chicken vasoactive intestinal peptide and porcine secretin were agonists of porcine vasoactive intestinal peptide with a 6-times and a 120-times lower potency, respectively. Among secretin analogs that were found to have low affinity for vasoactive intestinal peptide binding sites, [4-alanine, 5-valine]secretin, that resembles vasoactive intestinal peptide at the first seven amino acids at the N-terminal end, was a partial agonist of vasoactive peptide at the first seven amino acids at the N-terminal end, was a partial agonist of vasoactive intestinal peptide and others failed to stimulate cyclic AMP production. Glucagon (10microM), gastric inhibitory peptide (0.1 microM), substance, P, neurotensin, octapeptide of cholecystokinin, bovine pancreatic polypeptide, human gastrin I with leucine at residue 15, Leu-enkephalinand somatostatin (1 microM) did not alter cyclicAMP levels. Non-peptide mediators such as dopamine, serotonin, acetylcholine and histamine, tested at 10 microM, were also ineffective. Prostaglandins E2, E1 and isoproterenol, tested at 10 microM, induced an increase of cyclic AMP levels above basal but were 9.5, 13.7 and 17.5 times less efficient than vasoactive intestinal peptide, respectively. Thus vasoactive intestinal peptide is a unique stimulus of cyclic AMP production in rat intestinal epithelial cells.
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PMID:Interaction of vasoactive intestinal peptide with isolated intestinal epithelial cells from rat. 2. Characterization and structural requirements of the stimulatory effect of vasoactive intestinal peptide on production of adenosine 3':5'-monophosphate. 8 68

The effect of somatostatin on colonic secretion induced by 10(-8) M vasoactive intestinal peptide (VIP), 10(-2) M theophylline, and 2 X 10(-3) M dibutyryl cyclic AMP was studied in muscle-stripped everted open rat colon sacs. The secretory response to VIP, measured as the decrease in net absorptive flow rate (microliters 30 min-1 mg-1 of dry weight), was maximal and equalled the responses to theophylline or dibutyryl cyclic AMP. Somatostatin (10(-5) M) blocked completely the secretory response to VIP but only partially the secretory response to theophylline or dibutyryl cyclic AMP. This difference in the extent of inhibition suggested that somatostatin exerted an inhibitory effect both before and after the point of generation of intracellular cyclic AMP. In order to test the hypothesis that one component of the action of somatostatin involved inhibition of the production of cyclic AMP, measurements of this nucleotide were made in isolated rat colon cells. Control levels of cyclic AMP measured by radioimmunoassay (12.6 +/- 1.6 pmoles per 10(6) cells) were not affected by 10(-5) M somatostatin. VIP (5 X 10(-8) M) increased cyclic AMP levels 2-fold (P less than 0.01) and this increase was blocked by somatostatin. The results indicated that somatostatin inhibits colonic secretion by exerting effects at two sites: one site lies at, and another beyond, the point of generation of intracellular cyclic AMP.
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PMID:Inhibition of VIP-stimulated intestinal secretion and cyclic AMP production by somatostatin in the rat. 20 36

We have prepared 125I-labeled physalaemin and have examined the kinetics, stoichiometry, and chemical specificity with which the labeled peptide binds to dispersed acini from guinea pig pancreas. Binding of 125I-labeled physalaemin was saturable, temperature-dependent, and reversible and reflected interaction of the labeled peptide with a single class of binding sites on the plasma membrane of pancreatic acinar cells. Each acinar cell possessed approximately 500 binding sites, and binding of the tracer to these sites could be inhibited by physalaemin [concentration for half-maximal effect (Kd), 2 nM], substance P (Kd, 5 nM), or eledoisin (Kd, 300 nM) but not by cholecystokinin, caerulein, bombesin, litorin, gastrin, secretin, vasoactive intestinal peptide, glucagon, somatostatin, neurotensin, bovine pancreatic polypeptide, leucine-enkephalin, methionine-enkephalin, atropine, or carbamylcholine. With physalaemin, substance P, and eledoisin, there was a close correlation between the relative potency for inhibition of binding of labeled physalaemin and that for stimulation of amylase secretion. For a given peptide, however, a 3-fold higher concentration was required for half-maximal inhibition of binding than for half-maximal stimulation of amylase secretion, calcium outflux, or cyclic GMP accumulation. These results indicate that dispersed acini from guinea pig pancreas possess a single class of receptors that interact with physalaemin, substance P, and eledoisin and that occupation of 45% of these receptors will cause a maximal biological response.
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PMID:Interaction of physalaemin, substance P, and eledoisin with specific membrane receptors on pancreatic acinar cells. 23 Apr 88

Circulatory effects of gastrointestinal hormones and related peptides are surveyed. Only experiments using low peptide dosages, non-extensive surgery and intravenous infusions give relevant data in this field. Glucagon, secretin, vasoactive intestinal peptide, gastrin, cholecystokinin, Substance P and Somatostatin are vasoactive within the splanchnic area, each fraction in a specific pattern.
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PMID:Circulatory effects of gastrointestinal hormones and related peptides. 27 37

Using immunohistochemical techniques we studied duodenal biopsies from 18 patients with coeliac disease and 24 patients with normal duodenal morphology. We had access to antisera against the following gastrointestinal peptides: cholecystokinin (CCK), gastric inhibitory peptide (GIP), gastrin-17, glucagon-enteroglucagon, motilin, neurotensin, pancreatic peptide (PP), secretin, somatostatin, substance P and vasoactive intestinal peptide (VIP). The somatostatin, GIP, CCK, and glucagon cells were increased in number in coeliac disease. The number of motilin cells was slightly increased, while secretin cells were reduced. Cells storing gastrin-17, substance P, or neurotensin were rare in all patients regardless of diagnosis. No PP immunoreactive cells were found and VIP was localised to neurons only. In biopsies from patients having a mucosa with ridging of villi the number of the various endocrine cell types did not differ from that in the control group.
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PMID:Duodenal endocrine cells in adult coeliac disease. 38 55

Complementing cytochemical and ultrastructural studies, immunocytochemistry may be used to define, in terms of immunoreactivity, the nature of the polypeptide(s) made and stored in the cells of the endocrine pancreas, islet or otherwise. Immunoserums are applied to histological sections after fixation of the material in Bouin's fluid, and in accordance with four protocols: indirect immunofluorescence, immuno-enzymatic technique, variants in prolonged primary incubation and the method of soluble peroxidase-antiperoxidase complexes. Certain precautions are essential for correct interpretation. In the adult, four essential immunoreactions, corresponding to hormones or "local hormones" are regularly detected:insulin, pancreatic glucagon, somatostatin, pancreatic polypeptide. The cytochemical and ultrastructural characteristics of the cells involved are known (B, A and D cells for the first three specificities). C-peptide immunoreactivity is easily identified, but other immunoreactivities are more irregular or contested: gastrin, cholecystokinin, vasoactive intestinal peptide, ACTH, met-enkephalin.
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PMID:[Practical immunocytochemistry of the endocrine pancreas]. 39 37

We investigated in dogs the effect of graded frequencies of electrical vagal stimulation (1.5, 3, 6, and 12 cps) on pancreatic exocrine secretion and on portal blood levels of gastrin, secretin, cholecystokinin (CCK), vasoactive intestinal peptide (VIP), and somatostatin (STS). Stimuli of all four frequencies, each with a duration of 5 minutes, were applied with a secretin background of 0.25 CU/kg-hr, and one stimulatory period of 12 cps was applied without a secretin background. With secretin, a significant, frequency-dependent increase of volume and of pancreatic protein secretion occurred from 3 to 12 cps. Gastrin values increased significantly at all frequencies. VIP and STS increased significantly with 3, 6, and 12 cps. Maximal responses for gastrin, VIP, and STS were observed with 6 cps. Peak values for gastrin and VIP were found during stimulation, whereas STS peaked after the end of the stimulatory period. The integrated responses of gastrin and STS showed significant correlation (P less than 0.01). The results suggest that vagally induced pancreatic response is only partially mediated by gastrin and perhaps VIP, and that endogenous gastrin may be one of the releasing factors for somatostatin. Plasma levels of CCK and secretin did not change after electrical stimulation, which provides direct evidence that their release is unlikely to be under vagal control, and that CCK does not mediate the protein secretion obtained after electrical stimulation of the vagus.
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PMID:Effect of vagal stimulation on pancreatic secretion and on blood levels of gastrin, cholecystokinin, secretin, vasoactive intestinal peptide, and somatostatin. 46 78

When isolated rat liver cells were incubated in the presence of vasoactive intestinal peptide at the concentrations ranging from 0.2 microgram to 2 micrograms per ml, glycogenolysis was maximally stimulated within 15 min. However, somatostatin inhibited the liver glycogenolysis. The combined addition to the incubation medium showed that insulin and somatostatin inhibited the stimulated glycogenolysis induced by vasoactive intestinal peptide, while vasoactive intestinal peptide plus secretin showed no additive effect on glycogenolysis, as compared with single the addition of vasoactive intestinal peptide. On the other hand, the additon of glucagon to vasoactive intestinal peptide showed additive effects on glycogenolysis. These results suggest that the receptor site for vasoactive intestinal peptide may be distinguishable from that for glucagon. Extracellular calcium ions were demonstrated to play an important role in the modulation of vasoactive intestinal peptide-induced glycogenolysis. The evidence presented in this paper indicates that glucose metabolism may be partly regulated by the direct action of vasoactive intestinal peptide on hepatocytes, which is referred to as an enterohepatic axis and that the axis is inhibited by insulin and somatostatin.
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PMID:Effects of vasoactive intestinal peptide on glycogenolysis in cultured liver cells. 47 14

The effect of vasoactive intestinal peptide (VIP) was studied on the release of somatostatin (SRIF) from slices of several regions of the rat brain in vitro. VIP induced a dose-dependent inhibition of SRIF release from mediobasal hypothalamic slices but did not interfere with SRIF release from preoptic area, amygdala or cortex. VIP inhibition had an apparent affinity: Kd = 6.8 +/- 3.9 x 10(-11) M. Secretin had a similar effect but at 600-fold higher concentrations (Kd secretin = 4.2 +/- 0.6 x 10(-8) M). Gucagon was ineffective in concentrations ranging from 10(-10) M to 10(-7) M. The data are consistent with a role of VIP in the hypothalamic control of growth hormone secretion.
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PMID:Vasoactive intestinal peptide inhibits release of somatostatin from hypothalamus in vitro. 51 Mar 82


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