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)

This study was designed to test the effects of pentagastrin and epidermal growth factor (EGF) on stress-induced ulceration and on the antral content of gastrin and somatostatin (SLI) in rats. Four groups of 14 to 15 rats had been prepared for 7 days by one of the following methods: saline injection (control); injection of pentagastrin (250 micrograms/kg, 3 times/day); injection of EGF (10 micrograms/kg, 3 times/day); or injection of EGF plus pentagastrin. At the end of the treatment period, half of each group of rats were sacrificed (nonstress group). There were no ulcers in the nonstress control groups of rats. Stress was applied by water immersion in the remaining half of the rats. The injections of pentagastrin and/or EGF resulted in substantial increase in antral content of SLI. After 20 hours of stress, the ulcer index was 40.5 +/- 3.3 in the controls, compared to 6.4 +/- 1.2 and 16.2 +/- 2.3 in rats that received pentagastrin or EGF, respectively. Injections of both pentagastrin and EGF resulted in an ulcer index of 26.2 +/- 2.0, which was significantly lower than that in controls, but higher than that in rats treated with either peptide alone. The stress resulted in significant decrease in antral SLI in all groups of rats, whereas SLI content in rats treated with pentagastrin and/or EGF remained significantly higher than that of controls. Antral content of gastrin did not differ significantly in the four groups tested. The ulcer index was inversely correlated with antral SLI content. We confirm and extend previous observations that pentagastrin and EGF prevent stress ulcer formation, and suggest that endogenous SLI may account, at least in part, for their antiulcer activity.
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PMID:Cytoprotective effect of pentagastrin and epidermal growth factor on stress ulcer formation. Possible role of somatostatin. 285 83

Insulin, glucagon and somatostatin (SLI) in the pancreas and the gastrointestinal tissue of rats were measured following a high (300 mg/kg) or low (150 mg/kg) dose of cysteamine, given intermittently for 14 days. In addition, the effect of prolonged cysteamine-induced depletion of pancreatic SLI upon the cell distribution within the Langerhans islets was compared with that of chronic insulin-deficient rats produced by streptozotocin. The high or low dose of cysteamine reduced pancreatic SLI to 8.3% and gastrointestinal SLI to 5.6% of control levels without duodenal ulcer. The high dose of cysteamine also reduced pancreatic insulin to 37% of controls without hyperglycemia. No change in the glucagon concentration was observed. In SLI-deficient rats, distribution of A and B cells was similar to that of controls, even though D cells were rarely seen. In insulin-deficient rats, however, the number of A and D cells per islet area increased with a concomitant decrease in B cells. Intermittent administration of a low dose of cysteamine, thus, appears to be useful to produce a chronic SLI-deficient rat. However, a high dose of cysteamine is not a specific depletor of pancreatic SLI. Although insulin may be important to maintain normal cell distribution within the islets, pancreatic SLI may not have such a role.
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PMID:Effects of somatostatin deficiency on cell distribution within the Langerhans islets. 287 9

We studied the role of low plasma somatostatin (SRIF) levels in intestinal calcium absorption (CaA) in man. Plasma somatostatin-like immunoreactivity (SLI; pg X ml-1) rose after a 600-cal test meal (from 22.9 +/- 2 basally to 30.6 +/- 3.6 at 45 min, p less than 0.05), but was not affected by an oral Ca load (264 mg). Under intravenous SRIF (0.15 microgram kg-1 h-1) plasma SLI rose from 3.3 +/- 0.4 basally to 24.5 +/- 3 at 45 min (p less than 0.001). CaA was not influenced under these conditions, whereas insulin levels fell significantly and the levels of PTH, calcitonin, glucagon and GH were not changed. A regulating role of SRIF in CaA seems therefore unlikely for human physiology, since neither SLI is influenced by an oral Ca load, nor is CaA changed under postprandial SLI. The fall in insulin under postprandial-like SLI levels favors the view of a hormonal role of SRIF in man.
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PMID:Low-dose infusion of somatostatin in man--no effect upon intestinal calcium absorption but a fall in blood insulin. 287 94

We previously reported that the BB diabetic rat is characterized by a reduction in pancreatic immunoreactive somatostatin (SLI) content, delta-cell mass, and delta-cell secretory reserve. Despite this, portal plasma SLI levels are elevated in diabetic animals and normalized by insulin therapy. These findings comprise indirect evidence for SLI hypersecretion by the gut in untreated BB rats. This study was undertaken with isolated stomach perfusions to investigate directly the secretory status of gastric delta-cells in this diabetic model. Isolated stomachs of three groups of insulin-treated diabetic, untreated diabetic, and nondiabetic control rats were perfused in situ under basal and glucagon-stimulated (5 nM) conditions. Untreated diabetic BB rats exhibited significant enhancement of basal and glucagon-stimulated gastric SLI release. Insulin treatment reduced gastric SLI release to significantly subnormal levels. More than 95% of basal and stimulated SLI released in diabetic BB and normal control rats coeluted with synthetic somatostatin-14 on Sephadex G-50 columns. We conclude that basal and stimulated gastric SLI release is increased in untreated BB rats and is suppressed with insulin therapy, gastric delta-cell hyperfunction accounts for portal vein hypersomatostatinemia characteristic of untreated diabetic BB rats, and somatostatin-14 is the main molecular form of SLI released from normal and diabetic stomachs.
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PMID:Hypersecretion of gastric somatostatin in spontaneously diabetic BB rats. 288 58

The present study was designed to determine whether somatostatin is released into the circulation in sufficient amounts to regulate exocrine and endocrine pancreatic function and to evaluate the possible role of somatostatin as a hormonal regulator of the pancreas. Mean plasma somatostatin levels (SLI) increased from 11 +/- 2 pmol liter-1 to peak concentrations of 18 +/- 2 in six healthy male volunteers after a steak meal (P less than 0.05). Infusion of somatostatin inhibited hormone-induced exocrine pancreatic secretion and suppressed cerulein-stimulated pancreatic polypeptide (PP) secretion, but did not significantly change arginine-stimulated insulin and glucagon release at mean plasma somatostatin concentrations within the range seen after a meal. The amount of somatostatin released after a meal thus was of sufficient magnitude to inhibit exocrine pancreatic function and PP release. On the other hand, basal and arginine-stimulated glucagon and insulin secretions were not significantly affected by these plasma concentrations of intravenous somatostatin suggesting that the exocrine pancreas might be more sensitive to somatostatin than the islet cells. We conclude that somatostatin in concentrations within the range seen after a meal is a potent inhibitor of stimulated acinar cell function in man. The findings support the hypothesis that somatostatin acts as a true hormonal regulator.
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PMID:Circulating somatostatin. Physiological regulator of pancreatic function? 288 33

In the present study the effect of indomethacin-induced prostaglandin deficiency was examined on the release of bombesin-like immunoreactivity (BLI), a putative peptidergic neurotransmitter, from the isolated perfused rat stomach. In addition, gastrin and somatostatin (SLI) secretion was determined. Pretreatment of rats with indomethacin (2 mg/kg X h) resulted in a 3-fold increase of basal BLI secretion. In response to acetylcholine (2 X 10(-6) M) BLI rose from 2,000 to 4,000 pg/min, whereas in controls BLI increased from 400 to 1,400 pg/min. While absolute values for BLI secretion were higher in indomethacin-treated stomachs the relative increase above baseline was lower (100 vs. 250%). In control rats the increase in BLI secretion in response to acetylcholine was abolished when the acidity in the gastric lumen was increased from pH 7 to pH 2. After indomethacin, however, the stimulatory effect of acetylcholine during luminal pH 7 and pH 2 was identical. The decrease of SLI by acetylcholine at luminal pH 7 was abolished in indomethacin-treated stomachs in response to 10(-6) M acetylcholine, and 2 X 10(-6) M had even a stimulatory effect on SLI secretion. Indomethacin pretreatment reduced gastrin secretion at luminal pH 7. These data demonstrate that endogenous prostaglandins exert an inhibitory tone on basal and stimulated BLI and stimulated SLI secretion in the rat stomach. It is suggested that endogenous prostaglandins also inhibit the release of a peptidergic neurotransmitter, similar to their effect on the classical neurotransmitters acetylcholine and norepinephrine.
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PMID:Effect of indomethacin on bombesin-like immunoreactivity, somatostatin and gastrin secretion from rat stomach. 288 61

Several neuropsychiatric illnesses, including depression and Alzheimer's disease, are reported to be characterized by hypercortisolemia and by reduced levels of cerebrospinal fluid somatostatin-like immunoreactivity (CSF-SLI). To investigate a possible causal linkage between these abnormalities we administered prednisone, 80 mg orally per day for 5 days, to 9 healthy volunteers. We observed significant prednisone-induced reductions in CSF-SLI. Moreover, the magnitude of these reductions was inversely related to the magnitude of prednisone-induced reductions in plasma ACTH levels, suggesting a functional interaction between circulating corticosteroids, central somatostatin and pituitary ACTH release.
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PMID:Prednisone decreases CSF somatostatin in healthy humans: implications for neuropsychiatric illness. 288 25

Immunofluorescent staining for neuropeptide Y (NPY) in canine pancreatic tissue was performed together with an evaluation of the effects of synthetic NPY on the release of insulin (IRI), glucagon (IRG) and somatostatin (SLI) from the duodenal lobe of the canine pancreas in situ. NPY-like immunoreactivity was localized in perivascular nerve fibers throughout the acinar tissue. NPY-immunoreactive fibers were also demonstrated in the islets, usually surrounding blood vessels but also occasionally in fibers associated with endocrine cells, primarily at the periphery of islets. In addition, the ganglia dispersed in the pancreatic parenchyma were densely innervated by NPY-immunoreactive fibers, and these ganglia regularly contained cell bodies staining for NPY. Direct infusion of NPY into the pancreatic artery (p.a.) produced a dose-dependent decrease of pancreatic SLI output and of pancreatic venous blood flow. Low-dose p.a. infusion of NPY (50 pmol/min) had no effect on basal IRI or IRG output or on the islet response to glucose (5-g bolus, i.v.). High-dose p.a. infusion of NPY (500 pmol/min) transiently stimulated IRI output and modestly increased IRG output. However, the comparatively sparse innervation of canine islets with NPY-like immunoreactive fibers and the relatively minor effects of large doses of synthetic NPY on pancreatic hormone release lead us to conclude that this peptide is not an important neuromodulator of islet function in the dog.
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PMID:The presence and actions of NPY in the canine endocrine pancreas. 289 Jan 83

The possible role of different peptidergic systems in the postictal stage of human epilepsy was studied by measuring beta-endorphin, somatostatin, and prolactin levels by radioimmunoassay of cerebrospinal fluid (CSF) from nine epileptic patients. The first sample was taken within 2 hours after generalised tonic-clonic convulsion, and the second sample was obtained interictally after 1-4 days without any kind of clinically observable seizures. beta-endorphin was elevated postictally (p = 0.044) compared with interictal levels. SLI and PROL were similar in both samples. The present study suggests that in humans beta-endorphin is released into CSF during generalised seizures. This may indicate that neurons containing beta-endorphin are activated during a seizure.
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PMID:Beta-endorphin, somatostatin, and prolactin levels in cerebrospinal fluid of epileptic patients after generalised convulsion. 289 Jul 16

In response to insulin-induced hypoglycemia (0.1 U insulin/kg body weight, i.v.) plasma levels of growth hormone-releasing hormone (GHRH), somatostatin (SLI), and growth hormone (GH) were measured by radioimmunoassay in 10 children with short stature. Insulin injection resulted in a significant increase in plasma GHRH values at 15 min (10.0 +/- 0.5 vs. 17.1 +/- 3.1 pg/ml; p less than 0.05) preceding the increase in plasma GH levels (1.5 +/- 0.4 vs. 13.6 +/- 1.2 ng/ml; p less than 0.001). SLI concentrations peaked between 15 and 60 min after insulin injection (20.9 +/- 1.2 vs. 47.1 +/- 6.2 pg/ml; p less than 0.01). No correlation was present between plasma GHRH or SLI levels and plasma GH concentrations. A significant negative correlation could be established between maximum increments of plasma GHRH and SLI levels (r = -0.843; p less than 0.01) in response to insulin injection. This finding suggests a possible relationship between these two hormones at peripheral level.
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PMID:Effect of insulin-induced hypoglycemia on circulating levels of plasma growth hormone-releasing hormone and somatostatin in children. 289 99


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