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)

Spontaneously diabetic C57BL/6J obob and C57BL/Ks dbdb mice have been shown to have significantly decreased immunoassayable pancreatic somatostatin concentrations compared to lean littermate controls at 11-12 weeks: obob 1.06+/-0.15 pg/mug protein (n=10) vs control 1.94+/-0.-6 pg/mug protein (n=10) (mean +/- SE; p less than 0.005); dbdb 0.7+/-0.2 pg/mug protein (n=8) vs control 1.5+/-0.2 pg/mug protein (n=8) (mean +/- SE; p less than 0.005). An inverse relationship between circulating insulin levels and pancreatic SRIF concentration is suggested.
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PMID:Decreased pancreatic somatostatin (SRIF) concentration in spontaneously diabetic mice. 99 29

These studies were designed to elucidate the mechanism of inhibitory action of somatostatin (SRIF) on glucagon (IRG) and insulin (IRI) secretion. Studies were carried out in the unrecirculated isolated rat pancreas perfusion with arginine 19.2 mM and glucose 5.5 mM as stimulus primarily for IRG but also IRI secretion. The effects of excess Ca++ (15.2 mEq./L.) and excess K+ (12.8 mEq./L.) on IRG, IRI, and the SRIF-inhibited pancreas were studied. Ca++ excess in five perfusions strikingly stimulated IRG secretion (+92 per cent) but only stabilized IRI secretion compared with control perfusions. K+ excess (in seven perfusions) markedly inhibited IRG secretion (-39 per cent) while stimulating IRI secretion (+16 per cent). Restoration of normal concentrations of K+ resulted in a rebound of IRG to levels 120 per cent that of controls. SRIF, at concentrations from 0.1-20 ng./ml., produced inhibition of both IRG and IRI. In 11 perfusions, with SRIF at 10 ng./ml., IRG decreased more than IRI (-75.2 per cent IRG and -46.9 per cent IRI). In five perfusions, addition of Ca++ (15.2 mEq./L.) 10 minutes after SRIF was started resulted in a reversal of IRG inhibition to 69.4 per cent and IRI to 73.2 per cent of the arginine controls. The reversal by Ca++ of SRIF effect on IRG was greater at higher concentrations of Ca++, suggesting some form of competition. In four perfusions, excess K+ reversed SRIF-induced IRI inhibition to 79.6 per cent that of controls but had no effect on IRG inhibition. Studies in vitro with isolated islets revealed that SRIF (2 mug./ml.) inhibited 45Ca uptake of islets as did epinephrine (10(-5) M). It was concluded that SRIF-induced inhibition of hormone release appears related to an action on Ca++ uptake.
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PMID:Reversal of somatostatin inhibition of insulin and glucagon secretion. 99 24

The studies described were performed to develop a technically simple, yet sensitive in vivo model for growth hormone (GH) releasing activity in porcine stalk median eminence (pSME) extracts, to compare the GH releasing effects of pSME with those of prostaglandin E2 (PGE2), and to study the effect of somatostatin (SRIF) on the above stimuli. The use of the one day estrogen-primed male rat in conjunction with intracarotid injection of test materials provided a model sensitive to the injection of one pSME. Neither increasing the duration of estrogen pre-treatment nor reserpine resulted in a greater response. The GH releasing effects of pSME were directly related to the preinjection GH level. Two successive injections of pSME at 30 minute intervals evoked similar responses. In contrast, PGE2 effects were not potentiated by estrogen pre-treatment and were independent of the preinjection GH level. The GH releasing effect of pSME was not related to its content of TRH or K+. Extracts of porcine cerebral cortex also contained GH releasing activity, although at a lower concentration than in pSME. Somatostatin inhibited the GH releasing effects of pSME, PGE2, and cerebral cortex extract. These results provide evidence for the direct inhibitory effect of SRIF on GH secretion in vivo and suggest that SRIF is capable of blocking a variety of different stimuli to GH release.
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PMID:Effects of porcine stalk median eminence and prostaglandin E2 on rat growth hormone secretion in vivo and their inhibition by somatostatin. 109 73

Four analogs of ovine somatostatin (SRIF, PSOMATOTROPIN RELEASE INhibiting factor), the sequence of which is H-Ala-Gly-Cys-Lys-Asn-Phe-Phe-trp-Lys-Thr-Phe-Thr-Ser-Cys-OH, have been synthesized by the solid-phase methodology. The compounds were assayed and were found to possess the following somatotropin release inhibiting potencies relative to pure synthetic somatostatin in vitro and in vivo, respectively: [Ala3,14]somatostatin, 0.6 and 2.0%; [SMe-Cys3,14]somatostatin, 4 and 0.6%; [NAc-Cys3]somatostatin, 39 and 105%; [des-Ala1-Gly2]somatostatin, 65 and 71%. The dihydrosomatostatin analogs [NAc-Cys3-H2]somatostatin and [des-Ala1Gly2-H2]somatostatin after two purifications by gel filtration were assessed to be at least 80% homogeneous and had respectively 99 and 89% of somatostatin potencied in vivo. Structure-activity relationships are discussed.
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PMID:Somatostatin analogs. Relative importance of the disulfide bridge and of the Ala-Gly side chain for biological activity. 109 34

In order to determine the precise localization of somatostatin (SRIF) in the pancreas, electron microscopic immunocytochemistry was performed on thin sections of whole pancreas and isolated pancreatic islets of the rat using the peroxidase anti-peroxidase technique. SRIF was localized in secretory granules concentrated in cells sparsely distributed near the periphery of the islet. The granules were closely applied to their limiting membrane, exhibited moderate electron density, and were smaller than those in other islet cells. The location and relative number of SRIF-containing cells as well as the morphology of the granules suggest that SRIF is present in delta cells or a subgroup with small granules. These results provide evidence that SRIF is present in a discrete granule population in a specific type of secretory cell in the pancreatic islets.
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PMID:Ultrastructural localization of somatostatin in pancreatic islets of the rat. 110 49

Somatostatin was infused intravenously over two hours to rabbits in a dose of 1.5 mug/kg min with an initial loading dose of 50 mug/kg. This dose inhibited platelet aggregation in response to both ADP and collagen. Lower doses of SRIF had no effect. The addition of SRIF in vitro to either human or rabbit platelet rich plasma also had no effect on collagen or ADP-induced platelet aggregation.
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PMID:The effect of somatostatin on platelet aggregation. 117 21

Cell bodies of small to moderate-sized neurons in the female rat hypothalamus were stained specifically for somatostatin (SRIF) by means of the unlabeled antibody-peroxidase-antiperoxidase immunocytochemical method. SRIF-positive perikarya were scattered throughout the periventricular nucleus in a limited region extending from the middle of the optic chiasm to the rostral margin of the median eminence. The same neurons were revealed with either rabbit (R) or guinea pig (GP) anti-SRIF antisera. Positive cell bodies were more readily assessed with GP antibodies because nonspecific background staining was much less with these than with R anti-SRIF. Positive perikarya were not observed in other hypothalamic nuclei and ependymal elements were also immunocytochemically negative.
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PMID:Immunocytochemical localization of somatostatin in cell bodies of the rat hypothalamus. 119 68

The interaction of insulin and glucagon during infusion of somatostatin (SRIF), which suppresses secretion of these hormones, was investigated in normal, postabsorptive, concious dogs. Hepatic glucose output (production) and over-all glucose uptake by the tissues was measured with 3-3H-glucose, administered by a priming injection along with a constant infusion. Infusion of SRIF (1.5-5.0 mug/min) for 90 minutes resulted in a moderate hypoglycemia associated with a decrease in glucose production. In some animals glucose production and plasma glucose levels returned to normal before the end of SRIF infusion. Glucose uptake tended to follow plasma glucose levels. Upon termination of SRIF infusion, glucose production and uptake and plasma glucose increased sharply.
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PMID:Interaction of somatostatin, glucagon, and insulin on hepatic glucose output in the normal dog. 124 72

Galanin has been reported to stimulate secretion of GH in humans and rats. Thus, to investigate whether the effect of galanin on GH release is the result of either a stimulation of GH-releasing factor (GRF) and/or an inhibition of somatostatin (SRIF) release, we have evaluated the action of galanin on the release of SRIF and GRF from median eminence (ME) fragments in vitro. The MEs from adult male rats were incubated in Krebs-Ringer bicarbonate-glucose buffer, pH 7.4, at 37 degrees C, in an atmosphere of 95% O2, 5% CO2 with constant shaking for 30 min. Medium was discarded and replaced by medium containing various concentrations of galanin (10(-10)-10(-7) M). Galanin stimulated SRIF and GRF release in a dose-related manner. This effect was significant at concentrations varying from 10(-8) to 10(-7) M. To determine the mechanism by which galanin stimulated SRIF and GRF release, MEs were incubated with pimozide (dopaminergic blocker), phentolamine (alpha-adrenergic blocker) or naloxone (opioid blocker), at concentrations of 10(-6) M, and the effect of galanin was then evaluated. Phentolamine and naloxone did not alter the stimulatory effect of galanin, but when galanin was tested with pimozide, the galanin-induced release of SRIF and GRF was blocked. To determine whether the effect of galanin is mediated through D-1 and/or D-2 dopamine receptors, selective antagonists of D-1 (SCH 23390) and D-2 receptors (domperidone) were used (10(-7) M) in the presence of galanin (10(-7) M).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of galanin on growth hormone-releasing factor and somatostatin release from median eminence fragments in vitro. 128 34

Murine Monoclonal antibodies (MAbs) to the rat brain somatostatin (SRIF) receptor were produced. Sp 2/0 myeloma cells were fused with splenocytes of Balb/c mice immunized with the soluble rat brain SRIF receptor which was partially purified by gel-filtration chromatography. Screening by radioligand ([125I-Tyr11]SRIF-14) binding inhibition assay yielded three stable cell lines producing IgG1, IgM, or IgA antibody. Autoradiographic study of the polyacrylamide gel electrophoresed under nondenaturing conditions revealed that these MAbs inhibited the ligand binding to the receptor, regardless of their incubation with the receptor prior to the ligand binding. The results suggest that the MAbs produced are the antibodies to the ligand binding site of the receptor, and bind to the receptor in competition with the ligand.
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PMID:Monoclonal antibodies to somatostatin receptor of rat brain. 129 56


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