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)

Increasing the extracellular K+ concentration to 71 mM causes a phasic release of growth hormone and efflux of 45Ca from perifused bovine pituitary cells. Verapamil (20 micron) partially inhibits the initial phase of growth hormone release and 45Ca efflux and completely inhibits the second phase. Somatostatin (1 microgram/ml) partially inhibits both phases of growth hormone release but does not modify 5+-induced 45Ca efflux. Incubation of pituitary cells in 71 mM K+ increases 45Ca incorporation; verapamil (20 micron) completely prevents, and somatostatin (1 microgram/ml) partially inhibits, the K+-induced increase in 45Ca incorporation. The results suggest that 71 mM K+ increases both calcium entry into the cells and calcium redistribution within them, and that verapamil only inhibits the K+-induced calcium entry. Somatostatin may inhibit calcium entry into tissue stores.
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PMID:Effects of somatostatin and verapamil on growth hormone release and 45Ca fluxes. 62 36

The mechanisms of somatostatin secretion from nerve endings were investigated using the rat median eminence and neurohypophysis in vitro. Determination of total immunoreactive somatostatin content yielded: 36 +/- 2,7 ng per median eminence and 0,74 +/- 0,09 ng per neural lobe. Upon increasing the external potassium concentration a significant rise in somatostatin release from both tissues was observed. (Neural lobe: from 0,86% to 7,4%, median eminence: from 0,09% to 0,47% of total content per 30 minutes). A significant increase in hormone output was also observed following electrical stimulation. The secretory response was abolished whenever external calcium was omitted or replaced by manganese. It is concluded that somatostatin secretion from median eminence and neural lobe in vitro shows two characteristics typical of a neurosecretory process: release upon membrane depolarization and dependence of this process on external calcium.
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PMID:[In vitro somatostatin secretion from the median eminence and the neurohypophysis]. 66 11

Somatostatin has been detected in the gastrointestinal tract and has been shown to have wide actions on gastrointestinal function. Using an isotope method with 51Cr as a stool marker, we have examined the absorption of 47Ca in 9 healthy volunteers with and without infusion of cyclic somatostatin (250 microgram/h for 2 hours). Both serum and faecal measurements show reduced 47Ca-absorption during somatostatin infusion, net absorption falling from 53.0 +/- 14% without to 40.4 +/- 13% with somatostatin. Possible explanations are discussed with special emphasis on the possibility of an inhibition of active calcium transport, which may be a more general mode of somatostatin action.
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PMID:The effect on intestinal calcium absorption of somatostatin in man. 67 55

The effect of haloperidol, a dopaminergic antagonist, on insulin and glucagon secretion was investigated using the isolated, perfused canine pancreas. Haloperidol at 4 X 10(-7) to 10(-5) mol/l caused a dose-dependent inhibition of glucagon release both at low (25 mg/100 ml) and high glucose concentrations (150 mg/100 ml). At the low glucose concentration insulin release was already maximally suppressed. At the high glucose concentration haloperidol (4 X 10(-7) to 10(-5) mol/1) also caused a dose-dependent inhibition of insulin release. Haloperidol (10(-5) mol/1) inhibited dramatically pancreatic A and B cell responses to isoproterenol (2 ng/ml), acetylcholine (1 mumol/1) and arginine (5 mmol/1). The inhibitory effect of haloperidol on both glucagon and insulin release could be eliminated by increasing perfusate calcium concentration from 1.3 to 8.8 mmol/1. These findings suggested that haloperidol blocks glucagon and insulin release in a somatostatin-like manner by affecting a fundamental step of the stimulus-secretion coupling, probably by interfering with calcium handling of the pancreatic A and B cells.
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PMID:Haloperidol, a dopaminergic antagonist: somatostatin-like inhibition of glucagon and insulin release from the isolated, perfused canine pancreas. 71 Jul 56

The effect of somatostatin on the insulin response to an acute intravenous glucose load was studied in five normal subjects before and after induction hypercalcaemia. In the normocalcaemic state, the insulin response to glucose was depressed by somatostatin. In the hypercalcaemic state, insulin responses to glucose in the presence of somatostatin, were partially restored and appeared to be related to the level of increment of serum ionized calcium. It is concluded that, in the human being, hypercalcaemia and somatostatin have opposite actions on glucose-stimulated insulin secretion.
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PMID:The effect of serum ionized calcium elevation on somatostatin inhibition of glucose-induced insulin release in humans. 74 92

Both insulin and glucagon release by monolayer cell cultures of newborn rat pancreas were increased when calcium concentration was raised from 1.8 mEq/1 to 7.2 mEq/1. In low calcium medium, the calcium ionophore A23187 (10 mug/ml) enhanced insulin and glucagon secretion. Incubation with somatostatin (1.0 mug/ml), which inhibited hormonal release in a low calcium environment, paradoxically caused augmented insulin and glucagon secretion when A23187 was also present.
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PMID:Somatostatin inhibition of insulin and glucagon secretion in rat islet culture: reversal by ionophore A23187. 76 17

Somatostatin (1 mug/ml) inhibited glucose (16.7 mM)-stimulated 45Ca uptake by isolated rat islets incubated in media containing no added calcium or calcium at a low concentration (0.2mM). Epinephrine (50 mug/ml) and mannoheptulose (20mM) also inhibited 45Ca uptake by islets incubated in the presence of calcium (0.2mM). Addition of glucose (16.7 mM) caused a small but significant increase in insulin release from islets incubated in media containing no added calcium. In the presence of a low concentration of calcium (0.2 mM), glucose caused a much greater increase in insulin secretion which was inhibited by addition of somatostatin, epinephrine or mannoheptulose.
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PMID:Inhibition of calcium uptake by somatostatin in isolated rat islets of Langerhans. 78 58

This study was undertaken to determine the effect of somatostatin on acute, orciprenaline mediated, beta-adrenergic stimulation of free fatty acids, blood glucose, insulin, and glucagon in healthy subjects. After orciprenaline and somatostatin insulin and glucagon decreased, whereas blood glucose and free fatty acids increased, probably in part as a result of the lesser inhibition of glucagon (50%) than of insulin (83%). From these observations it is tentatively concluded that the inhibitory effects of somatostatin on insulin and glucagon release in man are a consequence of beta-adrenergic receptor involvement. These effects are possibly mediated through increased destruction of cAMP, blocking of camp dependent secretion or impairment of calcium uptake.
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PMID:Somatostatin modulation of pancreatic glucagon, insulin, glucose and free fatty acids following beta-adrenergic stimulation. 87 45

Somatostatin inhibited insulin secretion stimulated by glucose, tolbutamide, glucose-theophylline, glucose-cytochalasin B, and calcium in monolayer cell cultures of neonatal rat endocrine pancreas. Both 2-deoxyglucose-inhibited glucose-induced insulin release and basal insulin secretion occurring at glucose 1.7 mM were further reduced by somatostatin. In the presence of somatostatin, 1.0 mug/ml, insulin secretion due to glucose, tolbutamide, or glucose-cytochalasin B were inhibited to levels below the basal secretion seen with glucose 1.7 mM. However, insulin secretion stimulated by calcium, and especially by glucose plus theophylline, remained considerably above basal insulin levels, even with somatostatin 1.0 mug/ml. For all stimuli except calcium, at lower concentrations of somatostatin (0.001-0.10 mug/ml) but not at somatostatin 1.0 mug/ml, increased stimulus concentration partially reversed inhibition by somatostatin. For calcium, even at somatostatin 1.0 mug/ml, insulin release was greater when the calcium concentration was raised. Since net calcium uptake by the beta cell or intracellular translocation of calcium within the beta cell from an organelle-bound pool to a cytoplasmic pool may trigger insulin secretion through interaction of calcium with the microtubular-microfilamentous system, we suggest that the inhibition by somatostatin of calcium influx would explain our findings.
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PMID:Somatostatin inhibition of glucose-, tolbutamide-, theophylline, cytochalasin B-, and calcium-stimulated insulin release in monolayer cultures of rat endocrine pancreas. 110 17

Somatostatin, the hypothalamic growth hormone release inhibitory factor (GHRIF), directly inhibits both the first and second phases of insulin secretion. The sensitivities of these two phases of insulin secretion to somatostatin differ remarkably. The first phase of secretion is approximately 25 to 50 times more sensitive to somatostatin inhibition than is the second phase. In addition, somatostatin inhibition of insulin secretion during the second phase is "reversed" by supplemental calcium, whereas the somatostatin effect on the first phase is unaffected by additional calcium. These findings suggest that the cellular events which produce the two phases of insulin secretion are separate processes, and that somatostatin has a dual mechanism of action in inhibiting insulin secretion.
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PMID:Does somatostatin inhibition of insulin secretion involve two mechanisms of action? 110 17


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