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)

Previous exposure to glucose enhances insulin and depresses glucagon secretion by the pancreas. We have investigated whether secretion of somatostatin is also influenced by a glucose priming effect. In perfused rat pancreas from 36 h fasted rats a 5 min pulse of arginine (8 mmol/l) rapidly elicited a peak of somatostatin release. A similar somatostatin response was evoked by a second, identical, pulse of arginine after perfusion with "basal" glucose (3.9 mmol/l) for 45 min. On the other hand when 27.7 mmol/l D-glucose, was administered for 20 min between arginine pulses, there was significant stimulation of somatostatin secretion. When arginine was re-introduced 15 min after the cessation of the pulse of elevated glucose the magnitude of the arginine-induced peak (min 0-2 of stimulation) was increased from 16.2 +/- 4.1 to 33.1 +/- 4.7 pg/2 min, p less than 0.01, relative to the first stimulation with arginine. None of these effects of glucose could be reproduced by D-galactose. The somatostatin response to arginine was higher in pancreata from fed than from 36 h fasted animals as was also basal release (22.8 +/- 5.0 vs 9.0 +/- 2.0 pg/min). In the fed state the response to the second pulse of arginine was however reduced by 50% after perfusion with "basal" glucose. This decrease in responsiveness was counteracted by perfusion with 27.7 mmol/l glucose for 20 min between the arginine pulses. It is concluded that previous exposure to an elevated concentration of glucose enhanced D-cell responsiveness to arginine in the fasted as well as the fed state.
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PMID:Previous exposure to glucose enhances somatostatin secretion from the isolated perfused rat pancreas. 611 82

The effects of somatostatin on oral glucose tolerance and on intestinal absorption of glucose and other nutrients have been studied in anaesthetised rats. Intravenous somatostatin (0.1-0.6 nmol/min) increased the rate of gastric emptying. After intraduodenal administration of glucose, the rise in peripheral plasma levels of the sugar was delayed, but finally exaggerated by somatostatin, which inhibited the insulin response. Absorption was evaluated by measuring the disappearance of radioactive nutrients from the lumen of a 'tied duodenojejunal loop'. At a luminal concentration of 4 mmol/l of 3-0-methylglucose, neither disappearance of the sugar from the lumen nor its appearance in plasma was affected by somatostatin. Passive transport of 3-0-methylglucose (100 mmol/l) was not significantly modified by somatostatin, although the appearance of the labelled tracer in plasma was delayed. Somatostatin had no significant effect on absorption of galactose (4 mmol/l), sucrose (40 mmol/l), leucine (4 mmol/l) or palmitate (0.1 and 0.4 mmol/l). These results show that somatostatin delays appearance of ingested sugars in peripheral plasma without direct effect on the absorption sites; this delay may result from changes in intestinal motility, enzyme secretion and splanchnic blood flow.
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PMID:Somatostatin and the intestinal transport of glucose and other nutrients in the anaesthetised rat. 612 43

In dogs gastric secretion induced by tetragastrin and pancreatic secretion induced by secretin and/or cholecystokinin were inhibited by somatostatin at doses of 0.06-1 microgram X kg-1 X h-1 and 0.06-1 microgram X kg-1 X 0.5 h-1, respectively. Inhibition was a linear function of the logarithm of dose. Basal and 2-deoxy-D-glucose-induced gastric acid secretion was also significantly inhibited by low doses of somatostatin. Results in this study differ from those reported previously by clarifying the action of somatostatin as follows. 1) The inhibitory effect of somatostatin on pancreatic protein secretion was significantly greater than that on water and bicarbonate production. Somatostatin was more effective on cholecystokinin- than secretin-induced pancreatic secretion. 2) Although gastric mucosal blood flow (MBF) was affected by somatostatin, the reduction of MBF was not the primary mechanism responsible for its inhibitory action. 3) The low doses of somatostatin used in this study significantly inhibited gastric and pancreatic secretion without affecting the basal plasma concentrations of insulin, glucagon, growth hormone, gastrin, or secretin in the dogs, suggesting that the inhibitory action was not mediated by changes or reduction in plasma concentration of these hormones.
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PMID:Action of somatostatin on stomach, pancreas, gastric mucosal blood flow, and hormones. 612 5

Pancreatic islets of neonatal were dissociated by collagenase and cultured for 3 days in the presence of Cytodex beads to allow attachment of the cells to these microcarriers. The bead-attached cells were packed in columns and superfused with a low bicarbonate medium using the same method that we had originally developed for dissociated anterior pituitary cells of the rat. The secretion of insulin, somatostatin, and glucagon by the cells was monitored by radioimmunoassays. The cells in the superfusion system responded as expected from experiments with islet and monolayer cultures of rat pancreas in vitro and in vivo. Increasing glucose concentrations in the superfusion medium increased the release of insulin and somatostatin (SS), whereas glucagon secretory rates remained constant or decreased. A dose-response curve was established between insulin release and D-glucose in which the ED50 of D-glucose for insulin was found between 1.5 and 2 mg/ml. The phosphodiesterase inhibitor, 3-isobutyl-methylxanthine (IBMX), significantly potentiated the insulin response to glucose. Various secretagogues such as IBMX, 8-bromo cyclic AMP, and L-arginine increased insulin, somatostatin, and glucagon secretory rates in an expected manner. The superfusion method offers the possibility to investigate the interactions of dissociated A-, B-, and D-cells and the dynamics of hormone release in short- and long-term in vitro experiments. The method is simple and avoids the problems of monolayer procedures, such as clustering of the cells and poor adherence of dissociated pancreatic islet cells to dishes.
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PMID:Superfusion of dissociated pancreatic islet cells attached to Cytodex beads. 613 17

We have developed a new short term in vitro system to examine hypothalamic somatostatin (SRIF) release. Hypothalamic cells were obtained from normal rats after trypsin or collagenase aided dispersion and released immuno-reactive (IR) SRIF which eluted in 3 molecular weight (MW) forms on gel chromatography. The smallest MW form, which constituted the major peak, co-eluted with synthetic cyclic 1-14 SRIF on gel and reverse phase high pressure liquid chromatography (HPLC). After 24 h in culture in medium containing heat inactivated fetal calf serum, cell viability was demonstrated by two techniques, (1) vital staining with trypan blue, and (2) incorporation of 32Pi into phospholipids. SRIF release was also studied at this time which was optimal in terms of responsivity of the cells to depolarizing stimuli. SRIF release increased in a time dependent manner, over 3 h. Membrane depolarization, induced either by potassium chloride 56 mM or ouabain (the Na+, K+-ATPase inhibitor) 10(-6) M or greater, markedly stimulated SRIF release. Incubation at 4 degrees C, or in the presence of EDTA 0.05 M or verapamil, the calcium channel blocker, 50 microM abolished these stimulatory effects. Glucose deprivation was induced by the addition of 2-deoxy-D-glucose (2-DG) to the experimental medium. 2-DG, at concentrations of up to 200 mg%, had no significant effect on SRIF release during incubation periods of up to 1 h.
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PMID:Somatostatin release from dispersed hypothalamic cells - effects of membrane depolarization, calcium and glucose deprivation. 613 93

Glucose exerts opposite effects upon glucagon and insulin release from the endocrine pancreas. Glucose uptake and oxidation were therefore compared in purified A- and B-cells. In purified B-cells, the intracellular concentration of glucose or 3-O-methyl-D-glucose equilibrates within 2 min with the extracellular levels, and, like in intact islets, the rate of glucose oxidation displays a sigmoidal dose-response curve for glucose. In contrast, even after 5 min of incubation, the apparent distribution space of D-glucose or 3-O-methyl-D-glucose in A-cells remains much lower than the intracellular volume. In A-cells, both the rate of 3-O-methyl-D-glucose uptake and glucose oxidation proceed proportional to the hexose concentration up to 10 mM and reach saturation at higher concentrations. Addition of insulin failed to affect 3-O-methyl-D-glucose or D-glucose uptake and glucose oxidation by purified A-cells. Glucose releases 30-fold more insulin from islets than from single B-cells, but this marked difference is not associated with differences in glucose handling. The rate of glucose oxidation is virtually identical in single and reaggregated B-cells and is not altered after addition of glucagon or somatostatin. It is concluded that the dependency of glucose-induced insulin release upon the functional coordination between islet cells is not mediated through changes in glucose metabolism.
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PMID:Differences in glucose handling by pancreatic A- and B-cells. 614 Nov 62

The effects of D-glucose on the differential secretion of glucagon-like (GLI) and somatostatin-like (SLI) immunoreactivity have been studied using the perfused eel pancreas. During control perfusions with 2.7 mM glucose, basal secretion of GLI and SLI remained essentially stable for a period of 46 min, with an overall mean rate of 381 +/- 20 and 268 +/- 23 pg/min/100 mg dry wt of pancrease, respectively. An acute increase in perfusate glucose to 8.3, 16.7, and 33.3 mM resulted in a monophasic, dose-dependent decline in GLI secretion over 30 min. However, acute return of control glucose concentrations (2.7 mM) from 16.7 or 33.3 mM did not result in return of GLI to control levels, whereas from 8.3 mM glucose this was achieved slowly. By contrast, 8.3 mM glucose was without effect on SLI secretion, but at 16.7 and 33.3 mM a dose-dependent, biphasic pattern of release was evident, with a rapid return to control SLI levels during the terminal perfusion period with 2.7 mM glucose. The results suggest that the A and D cells of teleosts are sensitive to changes in glucose concentration, and, in terms of secretory profiles, release of GLI, and SLI, are qualitatively similar to those of mammals.
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PMID:Differential secretion of glucagon-like and somatostatin-like immunoreactivity from the perfused eel pancreas in response to D-glucose. 614 8

In the rat, hypoglycaemia inhibits growth hormone secretion, but the mechanism is unclear. To investigate this further, we have studied the effects of glucose and 2-deoxy-D-glucose on somatostatin and LHRH release from rat hypothalamic fragments incubated in vitro. Glucose (1.35-22 mM) was added to glucose-free medium and 5 and 50 mM 2-deoxy-D-glucose were added to medium containing 5.5 mM glucose. Medium somatostatin and LHRH levels were measured by RIA. Somatostatin and LHRH released diluted in parallel with synthetic somatostatin and LHRH. Sephadex gel filtration demonstrated two molecular forms of somatostatin, 70% coeluting with somatostatin-14 and 30% with somatostatin-28; LHRH coeluted with synthetic LHRH. KCl (30-100 mM) resulted in release of somatostatin and LHRH; this was reduced in calcium-free medium. Basal and K+-stimulated somatostatin release were significantly increased by reducing glucose levels (r = -0.6, p less than 0.001). Basal LHRH was not influenced by glucose. Basal and K+-induced somatostatin release were significantly increased by 2-deoxy-D-glucose (p less than 0.05), while LHRH levels remained unchanged. Our results demonstrate that basal and K+-induced somatostatin release from rat hypothalamic fragments are modulated by local glucose concentrations, and this effect is specific as it is not paralleled by LHRH changes. We suggest that the reduction in growth hormone secretion during hypoglycaemia in the rat might be mediated, at least in part, via a direct effect of glucose on somatostatin release.
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PMID:Glucose modulation of somatostatin and LHRH release from rat hypothalamic fragments in vitro. 614 38

The 22-residue somatostatin (SST-22) from channel catfish, purified by an improved method, is shown to be a glycopeptide. This represents the first report of a glycosylated somatostatin. Multiple forms of SST-22 exist with the major form containing 1 mol of galactose and 1 mol of N-acetylgalactosamine/mol of peptide attached via an O-glycosidic linkage to Thr-5. The position of the carbohydrate was determined by trapping the reactive peptide following beta-elimination of the carbohydrate with [35S]beta-mercaptoethanol followed by sequencing of the radiolabeled protein. All forms of SST-22 that have been purified are identical in amino acid composition. The heterogeneity resides in the carbohydrate portion of the glycopeptide with at least one of the minor forms containing sialic acid. The sequence for SST-22 obtained by automated Edman degradation is Asp X Asn X Thr X Val X Thr X Ser X Lys X Pro X Leu X Asn X Cys X Met X Asn X Tyr X Phe X Trp X Lys X Ser X Arg X Thr X Ala X Cys. This sequence differs at positions 5 and 19 from that published by Oyama et al. (Oyama, H., Bradshaw, R. A., Bates, O.J., and Permutt, A. (1980) J. Biol. Chem. 255, 2251-2254). The amino acid sequence reported here is identical to that deduced from the cDNA. The mass ion of SST-22 was determined by fast atom bombardment/mass spectrometry and shown to be 2943 +/- 1 (m/z). The observed mass ion is consistent with the molecular weight predicted from the amino acid sequence plus 1 mol of galactose and 1 mol of N-acetylgalactosamine.
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PMID:Structure of the 22-residue somatostatin from catfish. An O-glycosylated peptide having multiple forms. 614 20

Insulin-induced hypoglycaemia, which stimulates gastric acid secretion, is associated with an increase in circulating somatostatin levels in man. In order to assess the mechanisms involved in this rise, six normal volunteers connected to a Biostator for continuous glucose monitoring were studied, on three separate occasions. On each occasion after basal blood sampling, 0.15 i.u./kg body weight of insulin was administered i.v. and further samples were obtained intermittently over 150 min. On one occasion, dextrose was infused by the Biostator to prevent hypoglycaemia, while on the other two, a constant infusion of either normal saline or the specific H2 antagonist cimetidine was administered. Insulin plus dextrose caused no significant changes in circulating somatostatin levels, whereas insulin plus saline was associated with a marked, sustained and significant rise in all subjects; insulin plus cimetidine also produced a rise but it was delayed; the area under the curve was significantly (P less than 0.05) greater with insulin plus saline than with insulin plus cimetidine. These results show that in man insulin itself does not stimulate somatostatin secretion directly, but indirectly via hypoglycaemia. Further, the inhibition of gastric acid secretion with cimetidine reduces somatostatin release during insulin-induced hypoglycaemia. This suggests that gastric acid may mediate somatostatin secretion associated with insulin-induced hypoglycaemia.
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PMID:Studies on the mechanisms of somatostatin release after insulin induced hypoglycaemia in man. 615 Jul 71


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