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 haemodynamic effects and clinical uses of drugs used in the management of patients with oesophageal variceal bleeding are reviewed. Vasoconstrictor agents (vasopressin, teripressin) alone or in combination with nitrates continue to be used for acute bleeding episodes, while somatostatin is an alternative. Alpha- and beta-adrenergic blocking drugs and vasodilators which lead to a sustained decrease in portal pressure can be used for the prevention of bleeding episodes, but despite numerous studies the pharmacological treatment of variceal bleeding remains controversial.
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PMID:Review: the pharmacological control of variceal bleeding. 297 62

The influence of somatostatin (a bolus injection of 250 micrograms i.v. followed by 6 micrograms/min for 40 min) on the plasma cyclic AMP, insulin, glucose and non-esterified fatty acid (NEFA) responses to i.v. adrenaline (0.07 micrograms/kg body-weight/min for 20 min) and the plasma cyclic AMP, insulin and glucose responses to a bolus injection of i.v. glucagon (0.01 mg/kg BW) were studied in normal subjects. Somatostatin suppressed the insulin response to glucagon and inhibited the insulin rebound observed on termination of adrenaline infusion. The plasma glucose response to glucagon was exaggerated by somatostatin, reflecting insulin deficiency. Neither the plasma glucose or plasma non-esterified fatty acid responses to adrenaline were influenced by somatostatin. Adrenaline produced a three-fold and glucagon a twenty-fold rise in plasma cyclic AMP and 15 min. This was not influenced by concurrent somatostatin infusion, indicating that somatostatin is not a universal inhibitor of hormone stimulated adenylate cyclase activity. This is supported by the failure of somatostatin to inhibit the metabolic actions of glucagon and adrenaline thought to be mediated by cyclic AMP.
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PMID:Influence of somatostatin on plasma cyclic AMP and metabolic substrate responses to i.v. adrenaline and glucagon in humans. 612 54

Epinephrine (0.1 micrograms.kg-1.min-1) was infused with or without somatostatin (0.1 microgram.kg-1.min-1) in six depancreatized dogs, studied under normo- and hypoinsulinemia to determine whether the participation of glucagon in epinephrine-induced hepatic glucose overproduction is governed by the degree of metabolic control. When normoglycemia was achieved by basal intraportal insulin replacement, insulin levels remained constant during the epinephrine infusion, and there was a twofold increase in extrapancreatic immunoreactive glucagon (eIRG) and glucose production (Ra). Although eIRG increments were prevented by somatostatin, the increase in Ra was undiminished, indicating that epinephrine can act independently of glucagon as in normal animals. During subbasal intraportal insulin infusion in the depancreatized dogs, insulin levels remained 35% lower than with basal replacement, and the animals were hyperglycemic. Epinephrine induced a similar twofold increase in eIRG as during normoglycemia, and again this rise was prevented by somatostatin. There was a significantly greater, threefold increase in Ra with epinephrine when the animals were hyperglycemic. This exaggerated response to epinephrine was not seen during eIRG suppression by somatostatin, suggesting that glucagon participated in the epinephrine-induced hepatic glucose overproduction when the depancreatized dogs were in poor metabolic control, as seen previously in alloxan-diabetic dogs. However, in the depancreatized, unlike in the alloxan-diabetic dogs, epinephrine-induced glucagon release was small. Thus, hypoinsulinemia appears to sensitize the liver to eIRG during epinephrine infusion. The fact that epinephrine induces hyperglycemia both in physiology and diabetes could indicate an important role in enhancing glucose transport in insulin-insensitive tissues.
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PMID:State of metabolic control determines role of epinephrine-glucagon interaction in glucoregulation in diabetes. 612 26

1. An insulin-producing cell line, RINm5F, derived from a rat insulinoma was studied. 2. The cellular content of immunoreactive insulin was 0.19 pg/cell, which represents approx. 1% of the insulin content of native rat beta-cells, whereas that of immunoreactive glucagon and somatostatin was five to six orders of magnitude less than that of native alpha- or delta-cells respectively. 3. RINm5F cells released 7-12% of their cellular immunoreactive-insulin content at 2.8 mM-glucose during 60 min in Krebs-Ringer bicarbonate buffer. 4. Glucose utilization was increased by raising glucose from 2.8 to 16.7 mM. There was, however, no stimulation of immunoreactive-insulin release even when glucose was increased from 2.8 to 33.4 mM. A small stimulation of release was, however, found when glucose was raised from 0 to 2.8 mM. 5. Glyceraldehyde stimulated the release of immunoreactive insulin in a dose-dependent manner. 6. At 20 mM, leucine or arginine stimulated release at 2.8 mM-glucose. 7. Raising intracellular cyclic AMP by glucagon or 3-isobutyl-1-methylxanthine stimulated release at 2.8 mM-glucose with no additional stimulation at 16.7 mM-glucose. 8. Stimulation of immunoreactive-insulin release by K+ was dose-related between 2 and 30 mM. Another depolarizing agent, ouabain, also stimulated release. 9. Adrenaline (epinephrine) inhibited both basal (2.8 mM-glucose) release and that stimulated by 30 mM-K+. 10. Raising Ca2+ from 1 to 3 mM stimulated immunoreactive-insulin release, whereas a decrease from 1 to 0.3 or to 0.1 mM-Ca2+ lowered the release. 11. These findings could reflect a relatively specific impairment in glucose handling by RINm5F cells, contrasting with the preserved response to other modulators of insulin release.
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PMID:Regulation of immunoreactive-insulin release from a rat cell line (RINm5F). 613 20

Epinephrine and TRH independently release TSH from rat anterior pituitary cells in primary monolayer culture (ED50, 11 and 5 nM, respectively; maximum responses, 80% and 110%, respectively). The effects of these compounds together are additive, even at concentrations at which each is maximally effective alone. Dopamine inhibited basal and epinephrine-stimulated TSH secretion by 25 +/- 5% (+/-SE; ED50, 50 +/- 9 nM in each case). Somatostatin was effective against epinephrine-stimulated, but not basal, TSH secretion (80 +/- 4% inhibition; ED50, 1 +/- 3 nM). The data show that epinephrine is a potential regulator of TSH secretion by its own action and via its interactions with TRH, dopamine, and somatostatin.
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PMID:Interactions among epinephrine, thyrotropin (TSH)-releasing hormone, dopamine, and somatostatin in the control of TSH secretion in vitro. 614 35

The metabolic responses to infusion of adrenaline (6 micrograms/min) and of noradrenaline (5 micrograms/min) for 120 minutes have each been studied in five normal males with and without concurrent somatostatin (250 micrograms/h). Adrenaline induced marked and sustained hyperglycaemia (maximal blood glucose at 75 min, 9.0 +/- 0.4 mmol/l) while noradrenaline induced only a mild and transient blood glucose rise. Blood lactate was elevated by adrenaline (2.57 +/- 0.47 mmol/l with adrenaline, 0.62 +/- 0.06 mmol/l with saline at 120 min, p less than 0.02). Pyruvate levels rose proportionately less so that the circulating lactate:pyruvate ratio was increased (16.6 +/- 1.3 with adrenaline, 11.4 +/- 0.9 with saline at 120 min, p less than 0.05). Lactate and pyruvate levels were unaffected by noradrenaline. Both catecholamines increased circulating non-esterified fatty acid (NEFA) and glycerol to peak at 30 min, while maximal 3-hydroxybutyrate concentrations were achieved at 50 min (0.26 +/- 0.07 mmol/l with adrenaline; 0.23 +/- 0.06 mmol/l with noradrenaline; 0.03 +/- 0.01 mol/l with saline, both p less than 0.05). Insulin levels were partially suppressed by noradrenaline, while a small rise in circulating insulin was observed with adrenaline which was also associated with a large rebound rise in insulin secretion on cessation of the infusion. Mild and transient hyperglucagonaemia was observed with adrenaline while stimulation of glucagon secretion was more sustained with noradrenaline. Somatostatin suppressed insulin, glucagon and growth hormone secretion and both magnified and prolonged the hyperglycaemic effect of adrenaline (maximal at 105 min, 11.3 +/- 0.5 mmol/l, p less than 0.01 versus adrenaline alone).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic effects of adrenaline and noradrenaline in man: studies with somatostatin. 614 42

The effect of elevated plasma epinephrine concentrations (approximately equal to 800 pg/ml) on ketone body kinetics was determined in postabsorptive normal subjects using primed-continuous infusions of 3-14C-acetoacetate. Infusion of epinephrine (60 ng/kg/min) resulted in a transient increase in total ketone body production to a maximum of 2.5-fold the basal rate within 45 min (P less than 0.01 versus controls). Ketone body uptake increased with a delay, compared with production, causing a 2.8-fold increase in total ketone body concentrations (P less than 0.05 versus controls). Plasma free fatty acid (FFA) and blood glycerol concentrations increased transiently during epinephrine; their course was similar to that of ketone body production. Epinephrine administration resulted in hyperglycemia, hyperlactatemia, and a modest increase in plasma insulin and glucagon concentrations. To assess epinephrine's effect on ketone body kinetics during lack of insulin, and to avoid epinephrine-induced alterations in plasma insulin and glucagon concentrations, epinephrine was also infused combined with somatostatin (6.5 micrograms/kg/h). During somatostatin infusion, epinephrine administration resulted in an enhanced and sustained elevation of total ketone body production from 4.4 +/- 0.8 to 15.1 +/- 1.2 mumol/kg/min (P less than 0.01 versus somatostatin alone). Ketone body concentrations increased markedly from 310 +/- 63 to 1763 +/- 137 mumol/L (P less than 0.01 versus somatostatin alone); the ketonemic effect was enhanced due to a 40% decrease of the metabolic clearance rate associated with somatostatin infusion. The increase in plasma FFA and blood glycerol concentrations during somatostatin-induced insulin deficiency was transiently enhanced by epinephrine, such that they increased to 3.2- and 5.6-fold their basal values after 45 min, respectively (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of epinephrine and somatostatin-induced insulin deficiency on ketone body kinetics and lipolysis in man. 614 45

In isolated hepatocytes of rats with advanced phosphate depletion (serum Pi in controls: 8.79 +/- 0.16 mg/dl; Pi depletion: 2.79 +/- 0.18 mg/dl), diminished gluconeogenesis is observed [controls: 247 +/- 21 nmol X (mg protein)-1 X (30 min)-1; Pi depletion: 174 +/- 15]. In vitro stimulation with glucagon (28 nmol/l) caused a significant rise of glucose production, fall in lactate production, and increase in cAMP content in controls, but did not change glucose or lactate production in Pi depletion despite significant stimulation of cAMP content. This defect was not corrected by pretreating Pi-depleted animals with somatostatin. Impaired basal and glucagon-stimulated glucose production by hepatocytes of Pi-depleted animals was not reversed by incubation in a medium with high Pi content. Insulin (17 nmol/l) did not influence glucose or lactate production in hepatocytes of control or Pi-depleted animals. Epinephrine (10(-6) M) caused a significant stimulation of glucose production in control animals which was inhibited both by phenoxybenzamine (10(-4) M) and propranolol (10(-3) M). Epinephrine-mediated increase of glucose production with pyruvate (10 mM) as substrate was reduced but still demonstrable in hepatocytes of phosphate-depleted animals in parallel with a significant rise of hepatocellular cAMP concentration. Various concentrations of bovine PTH1-34 failed to affect cAMP concentration, glucose or lactate production in Pi-depleted animals and glucose or lactate production in controls. Impaired basal and stimulated (glucagon and epinephrine) glucose production despite adequate cellular cAMP generation points to steps distal to adenylate cyclase as the cause of disturbed hepatic gluconeogenesis in phosphate depletion.
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PMID:Effect of phosphate depletion on gluconeogenesis in isolated rat hepatocytes. 614 23

We have developed a model to allow study of the release of somatostatinlike immunoreactivity (SLI) from gastric mucosal cells. Collagenase-dispersed canine fundic mucosal cells were separated by counterflow elutriation. SLI-containing cells were identified in the fractions with small cells (9-11 microns), and these fractions were plated onto collagen. After 2 days in culture, SLI content of the cells was maintained; SLI-positive cells, detected by peroxidase-antiperoxidase immunohistochemistry, comprised 70 +/- 6% (mean +/- SE, n = 6) of these cultured cells. Release of SLI from these cultures into the medium was determined by radioimmunoassay. Epinephrine, dibutyryl cAMP, and gastrin each stimulated SLI release in a time-dependent manner, with a steady rate of secretion maintained for 120 min of incubation. Both epinephrine and dibutyryl cAMP markedly potentiated the release of SLI stimulated by gastrin but were not themselves mutually potentiating. Upon Sephadex G-50 column chromatography of incubation medium and extracts of cultured cells, SLI eluted primarily in a single peak that cochromatographed with synthetic somatostatin tetradecapeptide. Our data suggest that gastrin and adrenergic stimuli act directly on canine fundic somatostatin cells and that potentiating interactions between secretagogues may be important modulating elements in somatostatin cell secretory function.
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PMID:Release of somatostatinlike immunoreactivity from canine fundic mucosal cells in primary culture. 614 97

Adrenergic regulation of insulin secretion in the chicken was studied using a perifused pancreas fragment preparation. Beta-adrenergic stimulation by 50 microM isoproterenol potentiated theophylline-stimulated insulin secretion. Glucose at 19.5 mM did not stimulate insulin secretion, a finding consistent with previous reports of chicken pancreas sensitivity in vitro. Pretreatment with 50 microM isoproterenol did not alter this glucose insensitivity. Alpha-adrenergic stimulation by 50 microM epinephrine in the presence of beta blockade by sotalol or by 50 microM phenylephrine did not alter insulin secretion. Inhibition of insulin secretion by somatostatin could be demonstrated, however. Epinephrine, 50 and 0.164 microM, potentiated theophylline-stimulated insulin release and at 50 microM stimulated insulin secretion as an off-response even in the absence of theophylline. It is concluded that adrenergic regulation of insulin secretion in the chicken is primarily mediated through beta-adrenergic receptors, resulting in stimulation of insulin secretion.
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PMID:Adrenergic regulation of insulin secretion from the chicken pancreas in vitro. 638 99


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