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)

Cysteamine (300 mg/kg) administered subcutaneously depletes pancreatic somatostatin to 36% of control levels, but does not alter pancreatic insulin or glucagon content. Although perfusion of pancreata from normal animals with glucose (300 mg/dl) markedly stimulated somatostatin release, pancreata from cysteamine-treated animals failed to secrete somatostatin in response to glucose. Cysteamine treatment was without effect on insulin and glucagon release under the conditions tested. The isolated perfused pancreas from the cysteamine-treated rat provides a model for further investigations into regulation of islet hormone release in the absence of stimulated somatostatin release.
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PMID:Cysteamine blocks somatostatin secretion without altering the course of insulin or glucagon release. A new model for the study of islet function. 613 50

Cysteamine administration to rats results in a marked depletion of hypothalamic somatostatin-14 (SS14) and a decrease of the potassium-evoked in vitro release of SS14 without a significant change in the content or release of somatostatin-28(1-12)-like immunoreactivity (SS28(1-12)-L1). Furthermore, cysteamine enhances the spontaneous release and markedly potentiates the potassium-evoked release of SS14 in the in vitro slice preparation. However, in vitro-administered cysteamine does not alter the spontaneous or potassium-evoked release of SS28(1-12)-LI. Immunohistochemical visualization of hypothalamic neuronal cell bodies and fibers following cysteamine administration shows a disappearance of the SS14 immunoreactive fibers and cell bodies with no apparent change in the SS28(1-12) immunoreactive fibers and cell bodies. These data suggest that, in rat hypothalamus, selective release of SS14 and SS28(1-12) can occur. The results are discussed in relation to possible sites of storage and release of the somatostatin-related peptides from synaptic nerve terminals.
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PMID:Evidence for selective release of somatostatin-14 and somatostatin-28(1-12) from rat hypothalamus. 614 98

Cysteamine (beta-mercaptoethylamine HCl) administration to rats induces a hypergastrinemia and a reduction in gastric tissue somatostatin content. The possibility that this reduction may contribute to the elevated gastrin levels has been investigated in the isolated perfused rat stomach. Cysteamine (1 mM) rapidly increased immunoreactive gastrin release to levels ranging between 41% and 125% above basal. Increasing the dose to 10 mM caused a 1148% increase in immunoreactive gastrin. Secretion of somatostatinlike immunoreactivity did not change. Perfusion of gastric inhibitory polypeptide (1 nM) induced a sustained increase in somatostatinlike immunoreactivity secretion and a transient rise in gastrin. Addition of 10 mM cysteamine during gastric inhibitory polypeptide perfusion caused a 300% increase in immunoreactive gastrin. These levels were lower than in response to cysteamine alone. The results demonstrate that cysteamine can stimulate immunoreactive gastrin secretion without any change in somatostatinlike immunoreactivity release. When somatostatinlike immunoreactivity secretion is stimulated by an agent such as gastric inhibitory polypeptide, the cysteamine-induced release of immunoreactive gastrin is attenuated, suggesting the presence of a functional linkage between somatostatin and gastrin under these conditions.
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PMID:Effect of cysteamine on secretion of gastrin and somatostatin from the rat stomach. 614 43

Cysteamine given three times within 8 h produced severe duodenal and gastric ulcers in female SIV rats. A pentobarbital anesthesia during the first 10 h prevented gastric ulcer formation without affecting duodenal ulcer. An additional 10 h lasting intragastric infusion with 0.6 ml/h Ringer containing 5 mmol/l of a mixture 3: 1 pure taurocholic and glycocholic acid or 20 and 50 mmol/l pure taurocholic acid in 0.2 N HCl did not reverse the protective effect of pentobarbital, e.g. incidence and intensity of gastric ulcer did not change. Treatment with somatostatin significantly reduced the intensity of duodenal ulcer. The inhibition of cysteamine-induced gastric ulcer formation by pentobarbital does not seem to be due to a possible inhibition of duodenogastric reflux but more likely to an inhibition of central nervous stress reactions by anesthesia.
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PMID:Effect of pentobarbital anesthesia and bile acids on cysteamine-induced duodenal and gastric ulcers in rats. 614 97

Cysteamine (CSH) administered as a single sc injection to rats produced rapid depletion of cerebrocortical Somatostatin-14 like immunoreactivity (S-14 LI) with a significant 48% reduction occurring within 5 min and maximum (72%) decrease at 4 h. The depletion of S-14 LI was associated with a 1.7 fold increase in Bmax of the cerebrocortical S-14 receptors 5 min after CSH administration and a concomitant but slower increase in the affinity of these receptors [dissociation constant (Kd) being 1.8- and 1.6-fold lower than the control at 30 and 60 min, respectively, post CSH]. Incubation of intact synaptosomes with 1 mM CSH at 37 C in vitro for 60 min also caused a rapid depletion of S-14 LI, but in contrast to the in vivo data, there was no change in the Bmax or Kd of the S-14 receptors for up to 30 min beyond which time a 2.8-fold decrease in the affinity of S-14 receptors was observed. Higher concentrations of CSH (greater than or equal to 10 mM) added during the incubation of synaptosomes in vitro completely abolished the specific binding of these receptors. The pituitary S-14 receptors were studied 30 min after CSH administration and unlike the cerebrocortical S-14 receptors at this time did not exhibit any change in Bmax or affinity. When added at the time of the binding assay CSH (1 mM) was without a direct effect on cerebrocortical as well as pituitary membrane S-14 receptors. Furthermore, addition of CSH at the time of binding assay did not destroy the integrity of [125I-Tyr11]S-14. It is concluded that administration of CSH to rats in vivo depletes brain S-14 LI and up-regulates synaptosomal S-14 receptors. Exposure of synaptosomes to CSH in vitro for 30 min also depletes S-14 LI but has no effect on S-14 receptors suggesting that S-14 receptor regulation by S-14 is an in vivo phenomenon or requires the intact cell. CSH has a direct inhibitory effect on S-14 receptor binding after prolonged in vitro incubation. Pituitary S-14 receptors unlike those in the brain are unaffected by S-14 LI depletion at least acutely.
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PMID:Cysteamine-induced depletion of brain somatostatin is associated with up-regulation of cerebrocortical somatostatin receptors. 614 17

Local injection of cysteamine into rat striatum resulted in a dose-dependent reduction in somatostatin-like immunoreactivity (SLI). The effect was seen at 1 h, and persisted for up to 72 h, but was reversible at 1 week. The maximal depletion of SLI was approximately 50%. Histologic damage was largely confined to the needle tract. Of interest was a depletion of SLI in the contralateral striatum beginning at 3 h and maximal at 72 h. Cysteamine induced depletion of striatal SLI was not accompanied by alterations in dopamine or serotonin metabolism. Cysteamine is a useful pharmacologic tool for local somatostatin depletion.
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PMID:Depletion of striatal somatostatin by local cysteamine injection. 614 24

Rats were kindled by intraperitoneal injection of pentylenetetrazol (PTZ) (30 mg/kg) every 48 h. Once kindled, animals received a single injection of cysteamine (200 mg/kg) and subsequent responses to PTZ were observed. Cysteamine, an agent which depletes brain somatostatin and suppresses kindled seizures in amygdaloid-kindled rats, markedly suppressed the severity of PTZ-induced seizures in PTZ-kindled rats as well. However, it did not alter the convulsive response of non-kindled rats to a submaximal convulsive dose (50 mg/kg) of PTZ. The results support a role for somatostatin in kindling.
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PMID:Cysteamine suppresses kindled seizures in pentylenetetrazol-kindled rats. 615 12

Cysteamine hydrochloride was administered to rabbits at doses ranging from 0.3 to 10 mg by two intravitreal injections 24 h apart. Retinal immunoreactive somatostatin concentrations were reduced by about 50% at 24 h following the second injection. At doses of 0.3-3 mg, there was no demonstrable effect on retinal concentrations of immunoreactive substance P or of dopamine. Ten milligrams of cysteamine produced non-specific retinal damage. Cysteamine injected locally into the retina is a relatively specific drug for depletion of somatostatin.
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PMID:The effect of cysteamine on immunoreactive somatostatin in the rabbit retina. 618 51

The populations of endocrine cells in pancreatic islets are subjected to striking fluctuations in their size when subjected to sustained stimulation and/or inhibition of their secretory activity. The stimulation of a specific endocrine secretion is followed by proliferation of its producing cell, a situation that is reversed after interruption or inhibition of the stimulus. Morphometric and cytological modifications of somatostatin and glucagon producing cells (D and A cells respectively) in the islets of Langerhans have been studied by electron microscopy, immunocytochemistry and morphometry in pancreas of rats submitted to the following experimental conditions: 1) Adrenalectomized (ADX), 2) ADX treated with hydrocortisone, 3) Diabetic and 4) Cysteamine (CSH) treated rats. In addition to ultrastructural changes, the populations of A and D cells were analyzed morphometrically applying a computerized system for light microscopy of paraffin sections immunostained with peroxidase-antiperoxidase (PAP) technique. Glucagon cell population displayed striking alterations in fine structural features and in the volume density in the different experimental conditions examined. By contrast, the cytological organization and the size of somatostatin cell population were little or not affected except in the diabetic rats where the massive degeneration of beta cells grossly distorted the structure of the islets. These observations led to the conclusion that the population of D cells constitutes a stable of endocrine system, at variance to the profound modifications occurring in A cells when they are submitted to various experimental conditions that stimulate or inhibit their secretory activity.
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PMID:Differential proliferation of somatostatin and glucagon cells in rat pancreatic islets submitted to various stimuli. 759 19

Eight crossbred wethers (51 +/- 2 kg BW), surgically fitted with abomasal cannulas, were used to determine the extent and time course of cysteamine (CSH)-induced depletion of somatostatin (SRIF) in abomasal tissue and associated changes in plasma metabolites, insulin, and growth hormone (GH). Cysteamine was administered as a single i.v. bolus (50 mg.kg BW-1 x 10 min-1) on d 0. Abomasal biopsies were obtained on d -7, -3, 0, 1, 3, and 10. On d 0, additional biopsies were taken at 2, 4, and 8 h after CSH administration. Jugular blood samples were collected over 8 h at 15-min intervals on d -2, 0, and 1. Cysteamine administration decreased (P < .05) tissue SRIF on d 0 (2, 4, and 8 h), 1, and 3; maximal depletion (42 to 55% of Pre-treatment; Pre-trt) occurred during the initial 24 h, returning to Pre-trt by d 10. Gel chromatography of pooled -7 d abomasal tissue extracts showed five peaks of SRIF immunoreactivity; the predominate peak eluted in the same position as synthetic SRIF-14. Plasma glucose, lactate, and NEFA concentrations increased (P = .001) after CSH administration and reached peak at 2 h after treatment and declined to Pre-trt concentrations by 24 h. Insulin increased (P = .001) to a maximum at h 4 and returned to Pre-trt by 24 h. Mean and baseline GH were higher (P < .07) on day of CSH administration, and pulse amplitude was lower (P < .10) on d 0 and 1. These data show that CSH rapidly reduces SRIF in abomasal tissue in a reversible manner; suggesting that CSH-treated sheep may provide a SRIF-deficient model for studying the physiological role of SRIF in ruminants.
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PMID:Cysteamine-induced depletion of somatostatin in sheep: time course of depletion and changes in plasma metabolites, insulin, and growth hormone. 760 57


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