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)

Release of endogenous somatostatin (SRIF) from the rat cerebral cortical slices incubated in Krebs-bicarbonate buffer was increased from the basal rate of 3.4 +/- 0.6% of the total SRIF content in 15 min at [K+]o = 5.6 mM, to 13.1 +/- 1.6% upon raising the [K+]o to 56.6 mM. The high-K+ evoked SRIF release was absent when Ca++ in the medium was replaced by Mn++. The isolated synaptosomes from rat cerebral cortex contain 13.2 +/- 3.1 ng SRIF/mg protein compared to 0.33 +/- 0.01 ng/mg protein in the cortical tissue as a whole, suggesting that nerve terminals are the main source of the peptide released upon membrane depolarization.
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PMID:High K+-induced release of somatostatin from the cortical preparation of rat brain. 44 13

Somatostatin (SRIF) given intravenously, either as a single bolus or as a 2 hr infusion caused a significant prolongation of partial thromboplastin time (PTT) and depressed platelet counts and platelet aggregation in the rat. Following daily injections of protamin-zinc SRIF for 2 weeks the platelet count returned to normal, PTT remained prolonged and platelet aggregation was enhanced. The doses of SRIF used in this work were adequate to suppress the secretion of insulin and glucagon by the isolated pancreatic islets of treated animals.
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PMID:Somatostatin-induced changes in the hemostasis of rats. 46 25

Somatostatin (SRIF) is present in nerve endings in the median eminence (ME) and posterior pituitary. Hypothalamic SRIF containing neuronal perikarya are predominantly located in the anterior hypothalamic area (AHA), a region implicated in the inhibitory control of GH secretion. The effect of AHA lesions on SRIF in the ME, posterior pituitary, pancreas, stomach, and small intestine was studied in the rat in order to elucidate the source of ME and posterior pituitary SRIF and to determine if depletion of hypothalamic SRIF affects peripheral organ concentrations of the peptide. Lesioned animals showed a highly significant (P less than 0.01) 83% and 82% reduction in ME and posterior pituitary SRIF and to determine if depletion of hypothalamic SRIF affects peripheral organ concentrations of the peptide. Lesioned animals showed a highly significant (P less than SRIF concentrations in the pancreas, stomach, and small intestine of the lesioned animals. Plasma and pancreatic insulin and pancreatic glucagon were likewise unchanged. These data suggest that the hypothalamic SRIF pathway begins in the AHA, from where axons of somatostatinergic neurosecretory neurons project to both ME and posterior pituitary. AHA lesions have no effect on gut and pancreatic SRIF or pancreatic insulin and glucagon.
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PMID:Effect of anterior hypothalamic lesions on neurohypophysial and peripheral tissue concentrations of somatostatin in the rat. 46 31

To examine the roles of glucagon and insulin in exercise, four sheep were run on a treadmill with and without simultaneous infusion of somatostatin (SRIF), a peptide that suppresses glucagon and insulin secretion. SRIF infusion suppressed the exercise-induced rise in plasma glucagon during both moderate (5--5.5 km/h) and strenuous exercise (7.0 km/h). In addition, SRIF prevented the rise insulin concentrations during moderate exercise. During strenuous exercise, insulin concentrations were depressed in both groups. The infusion of SRIF was associated with a reduction in exercise-induced glucose production, as determined by infusion of [6-3H]glucose, during the first 15 min of both moderate and strenuous exercise compared to controls. Beyond 15 min glucose production was not significantly altered by SRIF infusions. These data are consistent with glucagon having an immediate, but only transient, stimulatory effect on the exercise-induced hepatic glucose production.
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PMID:Effect of somatostatin on plasma glucagon and insulin, and glucose turnover in exercising sheep. 46 84

Somatostatin-like immunoreactivity (SLI) is widely distributed in tissues and biological fluids. To determine whether SLI is also present in amniotic fluid, samples obtained by amniocentesis from 30 normal and 27 abnormal pregnancies were studied by radioimmunoassay. Direct incubation of [(125)I-Tyr(1)]tetradecapeptide somatostatin (SRIF) with amniotic fluid resulted in 89% tracer degradation. Damage was reduced to <5% when samples were acidified and boiled before the assay. With this technique, SLI was detectable in all normal amniotic fluid samples; the mean level at 15-20 wk of gestation (320+/-55 pg/ml, n = 15) being 4.5 times higher than the mean at 32-43 wk (70+/-12 pg/ml, n = 15) (P < 0.001). In cases of preeclampsia (n = 6), gestational diabetes (n = 5), anencephaly (n = 1), and meningomyelocele (n = 1), SLI values were in the normal range, but in one juvenile diabetic and one patient with chronic renal failure, SLI was undetectable (<10 pg/ml). In a pair of monochorionic diamniotic twins, SLI levels were very different (33 and 197 pg/ml), which suggests that fetal factors are more important than materno-placental ones in determining amniotic fluid SLI. Serial dilutions of amniotic fluid showed parallelism with standard SRIF. When concentrates of pooled amniotic fluid were chromatographed on Sephadex G-25 columns, all SLI eluted in the void volume ahead of SRIF even after treatment with 8 M urea and dithiothreitol. This "big" SLI incubated in amniotic fluid showed 100% stability over 24 h at 37 degrees C, whereas SRIF was rapidly inactivated (t((1/2)) congruent with 7 min). Extracts of placenta and fetal membranes contained no SLI, but small amounts (6-20% of total amniotic fluid SLI) were found in cells from fresh fluid. Radioimmunoassay of SLI in extracts of seven paired cord arterial and venous plasma samples showed no arteriovenous gradient consistent with fetal origin of cord blood SLI. It is concluded that (a) amniotic fluid contains SLI which is of fetal origin and (b) normal levels vary with gestational age. The SLI has a higher molecular weight (>/=5,000) and is more stable in amniotic fluid than SRIF.
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PMID:Measurement, characterization, and source of somatostatin-like immunoreactivity in human amniotic fluid. 46 88

Somatostatin was prophylactically administered to 10 patients who had surgery for pancreatic diseases. The postoperative course uncomplicated with no increase in serum amylase levels. Bile induced acute pancreatitis in six beagles was prophylactically treated with somatostatin. The results demonstrate that SRIF not only inhibits basal but also pancreatic-induced blood amylase and enzyme activities in the dog. SRIF-treated animals were in good general condition compared with untreated controls, macroscopic and histologic aspects of the pancreas were significantly improved.
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PMID:[Prevention of postoperative pancreatic complications following duodenopancreatectomy using somatostatin]. 47 69

The effect of somatostatin (SRIF) and of insulin on the plasma levels of immunoreactive glucagon (IRG) and glucose was examined in normal (N) and depancreatized (PX) dogs. The infusion of SRIF (3 microgram/min for 15 min) caused a rapid decrease of the total IRG measured by means of an antiglucanon serum (AGS 10) which cross reacts with extracts of intestinal mucosa. This decrease was due primarily to a fall in the IRG fraction measured by an antiserum (AGS 18) specific for the carboxyl terminus of pancreatic or A-cell IRG. When the dose of SRIF was increased to 10 microgram/min for 90 min, the difference between total and A-cell IRG in the systemic blood also decreased, indicating that other IRG fractions, such as gut IRG, had also been suppressed. The introduction of 50 ml of a 5% glucose solution into a loop of ileum was followed by an increase of gut IRG measured in the regional mesenteric blood. This response was suppressed by the infusion of SRIF (3 microgram/min). Insulin suppressed the basal level of total IRG, but did not alter the gut IRG response to glucose. The SRIF- and insulin-induced reduction in plasma IRG was not associated with a reduction in plasma glucose, suggesting that the high levels of total and A-cell IRG observed in depancreatized dogs were not essential for the maintenance of hyperglycemia.
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PMID:A-Cell and gut glucagon in normal and depancreatized dogs. Inhibition by somatostatin and insulin. 47 84

These studies assessed the ability of glucose infusions to potentiate the acute insulin response (AIR) to iv isoproterenol (12 micrograms), arginine (750 mg), or glucose (5 g) that was previously inhibited by an infusion of somatostatin (SRIF). SRIF (1.7 micrograms/min) markedly inhibited the AIR to isoproterenol (AIR before SRIF, 28 +/- 1 microU/ml; AIR during SRIF, 8 +/- microU/ml; P less than 0.025), arginine (AIR before SRIF, 6 +/- 2 microU/ml; AIR during SRIF, 1 +/- 1 microU/ml; P less than 0.01), and glucose (AIR before SRIF, 19 +/- 7 microU/ml; AIR during SRIF, 1 +/- microU/ml; P less than 0.05). The administration of a glucose infusion of 105 mg/min partially restored the AIR to isoproterenol and arginine. Glucose infused at 440 mg/min fully restored the AIR to both isoproterenol (AIR during SRIF plus glucose, 31 +/- 4 microU/ml) and arginine (AIR during SRIF plus glucose, 9 +/- 2 microU/ml). In contrast, the AIR to glucose was not affected by infusion of glucose (AIR during SRIF plus glucose, 0 +/- 1 microU/ml). In the absence of SRIF, glucose infusion potentiates the AIR to isoproterenol and arginine but not to glucose. Therefore, during SRIF infusion, glucose retains the ability to potentiate the AIR to nonglucose stimuli despite the loss of the ability to stimulate insulin release directly. These data suggest that the potentiating effects of glucose and the inhibiting effects of SRIF may be mediated by a common mechanism affecting insulin release.
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PMID:Glucose infusion potentiates the acute insulin response to nonglucose stimuli during the infusion of somatostatin. 48 8

The effect of hypophysectomy and bovine GH administration on somatostatin (SRIF) content in the rat hypothalamus was investigated. SRIF content was determined by a specific radioimmunoassay method described elsewhere. The total SRIF content of the rat hypothalamus as well as its content per milligram wet weight had decreased 4 weeks after hypophysectomy but was restored significantly in those rats which were subjected to bovine GH administration for 7 days 3 weeks after hypophysectomy. Furthermore, in nonoperated rats, increase of hypothalamic SRIF content was observed after 7 days GH administration. These results indicate that growth hormone may influence the SRIF content of hypothalamus and it seems likely that a feedback mechanism between pituitary GH and hypothalamic SRIF exists.
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PMID:Effect of hypophysectomy and growth hormone administration on somatostatin content in the rat hypothalamus. 49 79

The effect of somatostatin (SRIF) on glucagon and insulin secretion was examined in fed and fasted sheep. This was related to changes in glucose production. Infusion of SRIF at 80 micrograms/h caused a marked reduction in plasma glucagon concentrations. However, the insulin response to SRIF infusion was not consistent; its concentrations decreased occasionally, but often did not change. The depression of glucagon was not associated with a significant reduction in blood glucose concentrations in either fed or fasted sheep, but was associated with a reduction in glucose production by 12--15%. The inhibitory effect of insulin on glucose production was not markedly increased by glucagon deficiency. Infusion of insulin at 1.17 U/h with SRIF decreased glucose production only an additional 10%. Thus, it appears that under basal conditions pancreatic hormonal influences on hepatic glucose production were relatively small in sheep. This implies that under normal conditions in sheep, substrate supply has a much greater impact on hepatic glucogenesis than do hormones.
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PMID:Effect of somatostatin suppression of glucagon secretion on glucose production in sheep. 49 97


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