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)

The effects of somatostatin (growth hormone release inhibiting hormone) on basal gastrin were studied in patients suffering from pernicious anaemia and chronic renal and liver disease, and during sequential arginine/insulin-stimulated gastrin release in normal subjects. When basal gastrin concentrations were normal (10-50 pg/ml) in controls and in patients who were in renal and liver failure, somatostatin had no effect on gastrin levels. Raised basal gastrin levels in pernicious anaemia and in 2 cases of chronic renal disease, were significantly inhibited by somatostatin with a half-life (T 1/2) of 3-4 minutes. Arginine infusion caused an insignificant rise in serum gastrin which was unaffected by somatostatin, whereas insulin hypoglycaemia significantly stimulated gastrin release, which was inhibited by somatostatin.
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PMID:Somatostatin and serum gastrin in normal subjects and in patients with pernicious anaemia, chronic liver and renal disease. 117 34

The effect of the neuropeptide galanin on insulin and somatostatin secretion in the rat was studied under various conditions. In the perfused rat pancreas, insulin secretion stimulated by arginine, but not cholecystokinin-8 (CCK-8) or acetylcholine (ACh) was inhibited by both rat and porcine galanin, whereas ACh-stimulated somatostatin release was inhibited by rat but not porcine galanin. Neither arginine nor CCK-8 significantly altered somatostatin secretion and galanin was without effect under those conditions. Gastric inhibitory polypeptide-stimulated insulin release from cultured mixtures of purified rat beta- and non-beta-cells was inhibited by rat and porcine galanin in a concentration-dependent and equipotent manner. The results suggest that the inhibitory effect of galanin on insulin and somatostatin secretion may be stimulus-specific and species-specific.
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PMID:Stimulus-specific inhibition of insulin release from rat pancreas by both rat and porcine galanin. 128 Jul 55

Patients with hyperthyroidism have reduced GH responses to pharmacological stimuli and reduced spontaneous nocturnal GH secretion. The stimulatory effect of arginine on GH secretion has been suggested to depend on a decrease in hypothalamic somatostatin tone. The aim of our study was to evaluate the effects of arginine on the GH-releasing hormone (GHRH)-stimulated GH secretion in patients with hyperthyroidism. Six hyperthyroid patients with recent diagnosis of Graves' disease [mean age +/- SEM, 39.2 +/- 1.4 years; body mass index (BMI) 22 +/- 0.4 kg/m2] and 6 healthy nonobese volunteers (4 males, 2 females; mean age +/- SEM, 35 +/- 3.5 years) underwent two experimental trials at no less than 7-day intervals: GHRH (100 micrograms, i.v.)-induced GH secretion was evaluated after 30 min i.v. infusion of saline (100 ml) or arginine (30 g) in 100 ml of saline. Hyperthyroid patients showed blunted GH peaks after GHRH (13.2 +/- 2.9 micrograms/l) as compared with normal subjects (23.8 +/- 3.9 micrograms/l, p < 0.05). GH peaks after GHRH were only slightly enhanced by arginine in hyperthyroid subjects (17.6 +/- 2.9 micrograms/l), whereas, in normal subjects, the enhancement was clear cut (36.6 +/- 4.4 micrograms/l; p < 0.05). GH values after arginine + GHRH were still lower in hyperthyroid patients with respect to normal subjects. Our data demonstrate that arginine enhances but does not normalize the GH response to GHRH in patients with hyperthyroidism when compared with normal subjects. We hypothesize that hyperthyroxinemia may decrease GH secretion, both increasing somatostatin tone and acting directly at the pituitary level.
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PMID:Effect of arginine on the GHRH-stimulated GH secretion in patients with hyperthyroidism. 130 47

Nitric oxide has recently been implicated as the effector molecule that mediates IL-1 beta-induced inhibition of glucose-stimulated insulin secretion and beta-cell specific destruction. The pancreatic islet represents a heterogeneous cell population containing both endocrine cells (beta-[insulin], alpha-]glucagon], gamma[somatostatin], and PP-[polypeptide] secreting cells) and non-endocrine cells (fibroblast, macrophage, endothelial, and dendritic cells). The purpose of this investigation was to determine if the beta-cell, which is selectively destroyed during insulin-dependent diabetes mellitus, is both a source of IL-1 beta-induced nitric oxide production and also a site of action of this free radical. Pretreatment of beta-cells, purified by FACS with IL-1 beta results in a 40% inhibition of glucose-stimulated insulin secretion that is prevented by the nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (NMMA). IL-1 beta induces the formation of nitric oxide by purified beta-cells as evidenced by the accumulation of cGMP, which is blocked by NMMA. IL-1 beta also induces the accumulation of cGMP by the insulinoma cell line Rin-m5F, and both NMMA as well as the protein synthesis inhibitor cycloheximide prevent this cGMP accumulation. Iron-sulfur proteins appear to be intracellular targets of nitric oxide. IL-1 beta induces the formation of an iron-dinitrosyl complex by Rin-m5F cells indicating that nitric oxide mediates the destruction of iron-sulfur clusters of iron containing enzymes. This is further demonstrated by IL-1 beta-induced inhibition of glucose oxidation by purified beta-cells, mitochondrial aconitase activity of dispersed islet cells, and mitochondrial aconitase activity of Rin-m5F cells, all of which are prevented by NMMA. IL-1 beta does not appear to affect FACS-purified alpha-cell metabolic activity or intracellular cGMP levels, suggesting that IL-1 beta does not exert any effect on alpha-cells. These results demonstrate that the islet beta-cell is a source of IL-1 beta-induced nitric oxide production, and that beta-cell mitochondrial iron-sulfur containing enzymes are one site of action of nitric oxide.
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PMID:Interleukin 1 beta induces the formation of nitric oxide by beta-cells purified from rodent islets of Langerhans. Evidence for the beta-cell as a source and site of action of nitric oxide. 133 75

Pancreatic polypeptide (PP) secretory cells are abundant in the islets of Langerhans. Results concerning the effects of exogenous PP on islet-cell secretion are controversial. This might be due in part to species specificity, given that most reports refer to studies performed using PP of bovine, porcine, or human origin in a heterologous animal model. Thus, we have investigated the influence of synthetic rat PP (80 nmol/L) on unstimulated insulin, glucagon, and somatostatin release, and on the responses of these hormones to glucose (11 mmol/L) and to arginine (3.5 mmol/L) in a homologous animal model, the perfused rat pancreas. Infusion of rat PP (rPP) reduced unstimulated insulin release by 35% (P = .03), and the insulin responses to glucose by 65% (P = .029) and to arginine by 50% (P = .026), without modifying glucagon output. rPP did not affect somatostatin secretion, either in unstimulated conditions or in the presence of 11 mmol/L glucose. However, it induced a clear-cut increase in somatostatin release during 3.5 mmol/L arginine infusion. Our observation that rPP inhibited insulin secretion without affecting glucagon and somatostatin output points to a direct effect of PP on B-cell function. However, during aminogenic priming of the D cell, the inhibition of insulin output induced by rPP was accompanied by an increase in somatostatin release. Thus, in this circumstance, it might be considered that the blocking effect of PP on B-cell secretion could be, at least in part, mediated by a D-cell paracrine effect.
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PMID:Effects of rat pancreatic polypeptide on islet-cell secretion in the perfused rat pancreas. 134 99

Glucagon has been suggested to be a mediator of intra-islet paracrine effect of insulin and somatostatin during nutritive stimulation. The aim of this study was to reveal possible intra-islet interactions between insulin, somatostatin and glucagon in a batch stimulation model with isolated pancreatic islets. Such interactions may influence stimulus-secretion experiments in this experimental model. In our hands arginine stimulated somatostatin secretion only in the presence of insulin antiserum. Furthermore, arginine-induced glucagon secretion was greatly increased following addition of insulin antiserum. The addition of glucagon antiserum inhibited these effects of insulin antiserum on somatostatin secretion. In conclusion, glucagon apparently represents the central mediator of arginine effects on somatostatin secretion in isolated rat pancreatic islets in batch stimulation experiments.
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PMID:Glucagon mediates arginine-induced somatostatin secretion from isolated rat pancreatic islets. 135 Mar 74

This study examined the effects of exogenous somatostatin and insulin on the release of islet amyloid polypeptide (IAPP), or amylin, from the isolated perfused rat pancreas. Somatostatin inhibited the release of both amylin and insulin from the perfused pancreas to the same extent. The infusion of 10 nM somatostatin resulted in 40% inhibition of the secretion of both amylin and insulin induced by 11.1 mM glucose and 10 mM arginine, and this inhibition was significantly increased to 70% by the infusion of 100 nM somatostatin (p less than 0.05). The amylin/insulin molar ratios remained constant at 0.8% and were not changed by the infusion of somatostatin. On the other hand exogenous insulin at a concentration of 1.8 nM did not affect the release of amylin induced by 11.1 mM glucose and 10 mM arginine, whereas 180 nM insulin slightly, although not significantly, inhibited the release of amylin by 15%. These findings suggest that the release of amylin may be negatively regulated by somatostatin and that circulating insulin may have no direct effect on the release of amylin at least at a physiological concentration.
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PMID:Effects of exogenous somatostatin and insulin on islet amyloid polypeptide (amylin) release from perfused rat pancreas. 135 50

Acute hyperglycemia inhibits the growth hormone (GH) response to several stimuli including growth hormone-releasing hormone (GHRH), likely acting by stimulation of endogenous somatostatin release. The aim of our study was to verify whether arginine ([Arg] 30 g intravenously [IV] in 30 minutes), a well-known GH secretagogue likely acting via inhibition of hypothalamic somatostatin release, counteracts the inhibitory effect of oral glucose (OG) administration (100 mg orally) on the GH response to GHRH (1 micrograms/kg IV bolus) in seven normal subjects (aged 20 to 30 years). The GH response to GHRH (peak, 11.6 +/- 1.8 micrograms/L) was inhibited by previous OG load (peak, 7.4 +/- 0.8 micrograms/L; P less than .02 v GHRH alone) and potentiated by Arg coadministration (peak, 36.2 +/- 8.8 micrograms/L; P less than .03 v GHRH alone). The potentiating effect of Arg on the GHRH-induced GH increase was unaffected by previous OG load (peak, 30.4 +/- 6.9 micrograms/L). In conclusion, our results show that Arg abolishes the inhibitory effect of OG administration on the GHRH-induced GH response in man. These data, although indirect, suggest that both acute hyperglycemia and Arg act at the hypothalamic level, stimulating and inhibiting, respectively, the release of somatostatin.
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PMID:Arginine abolishes the inhibitory effect of glucose on the growth hormone response to growth hormone-releasing hormone in man. 135 80

This study examines the insulin response of pancreatic islets isolated from diabetic BB rats (BBD), nondiabetic BB rats (BBN), and Wistar rats to in vitro stimulation. After a 48-hour culture period, insulin release in response to glucose (17.8 mmol/L) either alone, with glucose-dependent insulinotropic polypeptide (GIP) +/- somatostatin (SS), or with Arg +/- SS was measured. A static incubation system was used. Insulin secretion from islets cultured in 4.4 mmol/L glucose (basal) did not differ between BBN and BBD rats (0.50% +/- 0.08%, 0.67% +/- 0.25% of total islet cell content [TCC], respectively). High glucose concentrations (17.8 mmol/L) stimulated a modest increase in insulin release from BBD and BBN islets (1.8% +/- 0.48% and 2.1% +/- 0.19% TCC, respectively). The addition of GIP (1 nmol/L) enhanced glucose-stimulated insulin secretion from BBN rat islets (2.9% +/- 0.42% TCC), but had no effect on BBD islets (2.04% +/- 0.57% TCC). Somatostatin (1 mumol/L) completely reversed the glucose- and/or GIP-stimulated insulin secretion from both BBN and BBD rat islets to basal levels (0.42% +/- 0.043%, 0.42% +/- 0.09% TCC, respectively). Arg (1 mmol/L) enhanced glucose-stimulated insulin secretion in both groups, although the greatest response was elicited from BBD rat islets (8.4-fold v 3.2-fold). Experiments comparing BB rats with Wistar rats demonstrated significant differences in the glucose-stimulated (17.8 mmol/L) insulin response of the islets. Islets taken from BBN and BBD were less responsive to glucose than those from Wistar rats. However, islets from BBD rats were hyperresponsive to Arg when compared with islets from Wistar rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin response of cultured islets from diabetic and nondiabetic BB rats. 135 29

The effects of short-term (90 min), mid-term (5 days), and long-term (15 days) administration of ammonium acetate (5 mmol/Kg day i.p.) on the somatostatinergic neurotransmitter system of the rat hippocampus have been studied. Scatchard analysis of the binding of 125I-Tyr11-somatostatin to hippocampal dissociated cells indicated that administration of ammonium acetate at the times studied were associated with a decrease in the number of somatostatin receptors in this brain area, whereas the affinity of the same receptors remained unchanged. Administration of ammonium acetate did not affect the levels of somatostatin-like immunoreactivity in the hippocampus. Treatment with N-carbamyl-L-glutamate (1 mmol/Kg, i.p.) plus L-arginine (1 mmol/kg), which lead to the conversion of ammonia into urea, prevented the ammonium acetate-induced changes in somatostatin binding in this brain area. N-carbamyl-L-glutamate plus L-arginine alone had no observable effect on the somatostatinergic system. The decrease in the number of somatostatin receptors induced by ammonium acetate might reflect a decreased sensitivity of the target cells to somatostatin, a phenomenon that could contribute to the depressed neuronal excitability induced by ammonia in the rat hippocampus.
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PMID:Somatostatin binding reduced by ammonium acetate in the rat hippocampus can be reversed by treatment with N-carbamyl-L-glutamate plus L-arginine. 135 63


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