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)

Hyperglycemia, hyperglucagonemia and hyperinsulinemia were observed in fasting rats at 0.5 hr after ip injection of NiCl2 (68 mumole per kg). Infusion of somatostatin iv (0.5 mg per rat) did not prevent Ni(II)-mediated hyperglycemia, hyperglucagonemia or hyperinsulinemia. Exposure of rats to inhalation of Ni(CO)4 (1.2 to 6.4 mumole per liter of air per 15 min) caused acute hyperglycemia, similar to that observed after ip injection of NiCl2. Hyperglycemia induced by NiCl2 and Ni(CO)4 was not associated with inhibition of erythrocyte glycolysis measured in vitro by erythrocyte uptake of 1-14C-glucose and release of 14CO2. These findings indicate that Ni-induced hyperglycemia may be mediated by increased pancreatic release of glucagon, but that Ni stimulation of glucagon release differs from stimulation of glucagon release by arginine or epinephrine, since the Ni effect is not antagonized by somatostatin.
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PMID:Effects of nickel chloride and nickel carbonyl upon glucose metabolism in rats. 73 12

The isolated perfused canine pancreas with duodenal exclusion was used to examine islet hormone output in response to arginine and exogenous glucagon and insulin. Exogenous glucagon (100 ng/ml) stimulated insulin and somatostatin secretion, which occurred in a biphasic pattern. The insulin response to glucagon was markedly enhanced by increased perfusate glucose, unlike the somatostatin response, which was little affected. The insulin and somatostatin responses were seen between 15 and 45 s after the glucagon stimulus. Pancreatic polypeptide secretion was uninfluenced by exogenous glucagon. Biphasic release of glucagon, somatostatin, and pancreatic polypeptide was evoked by 10 mM arginine, the responses first being apparent within less than 30 s. Exogenous insulin (50 mU/ml) infused for 10 min had no statistically significant effect on glucagon, somatostatin, or pancreatic polypeptide secretion. This study suggests that these four islet hormones may all be involved in the dynamic mechanisms of nutrient metabolism. In addition, potential intra-islet paracrine effects are identified.
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PMID:Somatostatin and pancreatic polypeptide secretion: effects of glucagon, insulin, and arginine. 75 49

Somatostatin, or SRIF (Somatotropin Release Inhibiting Factor), is a tetradecapeptide of hypothalamic origin, which inhibits the secretion of growth hormone. It has also been recognized in other parts of the central nervous system, in the islets of Langerhans, and the mucosa of the upper digestive tract. Parenteral administration of synthetic SRIF inhibits the release of growth hormone, basal and stimulated by muscular exercise, arginine, L-DOPA, insulin-induced hypoglycemia, and sleeping. It also inhibits insulin and glucagon secretion, basal and stimulated, and several other secretory processes in endocrine and exocrine glands. It may have a depressor effect on some neurons in the central nervous system. Considerable interest has been prompted in the field of diabetology by the demonstration of somatostatin-induced suppression of growth hormone and glucagon : both hormones are over-secreted in many diabetic patients, and both may be noxious for small blood vessels in the diabetic. The eventual therapeutic use of somatostatin in humans is restricted, for the moment, by the unavaibility of long-acting SRIF preparations and the possibility of some adverse effects mainly affecting hemostasis. Evaluation of the physiological role (s) for this newcomer, and of the eventual pathophysiology of endogenous somatostatin, represent an unexpected and exciting field of neuro-endocrinology.
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PMID:[Somatostatin, a new hormone? (author's transl)]. 79 89

Somatostatin and dihydrosomatostatin (H2somatostatin) are equipotent in inhibiting insulin and glucagon release induced by arginine in the rat. The ID50 of H2somatostatin on insulin and glucagon secretion induced by arginine are 14 +/- 6 and 6 +/- 10 mug/100 g BW respectively, similar to the ID50 of H2somatostatin (18 +/- 10 mug/100 g BW) on inhibition of insulin release induced by glucose. Thyrotropin releasing factor, luteinizing hormone releasing factor, alpha-MSH, and the N-terminus decapeptide of the beta-chain of porcine hemoglobin did not alter the secretion of insulin and glucagon induced by arginine. With the exception of [Ala2[-somatostatin and [Ala5]-somatostatin, alanine substituted analogs of somatostatin were less potent than somatostatin. [D-Trp8]-somatostatin is 6-8 times as potent as somatostatin in inhibiting insulin and glucagon release induced by arginine. The relative potencies of these analogs to inhibit the secretion of the pancreatic hormones are in good agreement with our previously reported values based on the inhibition of GH secretion in vitro.
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PMID:Biological activity of somatostatin and somatostatin analogs on inhibtion of arginine-induced insulin and glucagon release in the rat. 81 91

Plasma GH and cortisol responses were examined in unanesthetized adult male rhesus monkeys infused with approximately 30 ml (8.3 ml/kg) of arginine monohydrochloride (Arg 0.5 g/kg), 0.9% saline (NS) or Dextran 75 and following 15 ml infusions of acid-saline (AS), or somatostatin (GHRIH 30 mug/kg). None of the infusions were accompanied by GH elevations. Rebound GH elevations occurred after each 30 ml infusion and after GHRIH but not after 15 ml AS. Although the amplitude of GH responses were not significantly different (p greater than 0.05), responses to Arg and dextran were significantly delayed as compared to responses following NS and GHRIH which did not differ from each other. Both of the latter responses occurred within 15 min of infusion completion. The delay following dextran was significantly longer than that following Arg (p less than 0.05). Since the volume of saline and the dosage of Arg were equivalent to those used in the standard intravenous Arg test, results suggest that effects of infusion volume upon GH secretion and upon GH responses to Arg warrant examination in the human. In addition, it is suggested that GH responses to NS and to dextran are mediated via an intravascular volume control mechanism and that GHRIH may be released upon activation of such a mechanism. GH elevations may represent rebound responses upon termination of GHRIH secretion.
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PMID:Stimulation of rhesus monkey GH release: arginine vs plasma volume expansion. 81 33

Thirteen patients with acromegaly were subjected to the examination of autonomity in growth hormone (GH) secretion. TRH (500 mug iv), arginine (0.5 g/kg of body weight iv infusion), LH-RH (100 mug iv) and L-dopa (500 mg orally) were administered, and plasma GH was measured. Among them, 11 patients showed some response in plasma GH to at least one agent, but the other 2 cases showed no response to any of the above 4 agents. In the former 11 cases, the patients were regarded as belonging to the less autonomous type and in the latter 2, to the more autonomous type in GH secretion. Six cases (4 cases of the less autonomous and 2 cases of the more autonomous type) received an administration of 500 mug of synthetic somatostatin parenterally. Following administration of somatostatin, the patients of both types showed significant GH decrease, although GH decrease in the more autonomous type was smaller than that of the less autonomous type. These results would suggest that there might be no acromegalics secreting GH FROM THE PITUITARY WITH COMPLETE AUTONOMITY, AND THE DIFFERENCE OF AUTONOMITY IN ACROMEGALIC PATIENTS MIGHT DEPEND EITHER ON THE DIFFERENCE IN SENSITIVITY AND/OR THE NUMBER OF RECEPTORS IN THE PITUITARY RATHER THAN THOSE IN HYPOTHALAMUS TO EXOGENOUS STIMULI.
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PMID:Differences in autonomity of growth hormone secretion in patients with acromegaly. 82 58

A system consisting of an isolated dog stomach perfused with whole blood has been designed to study gastric glucagon secretion. Under basal conditions, gastric glucagon release was 0.0-3.1 ng glucagon/100g of stomach per min. Arginine, at an arterial plasma concentration averaging 10 mM, elicited a rapid glucagon release. This gastric glucagon release was almost completely abolished by somatostatin (100 ng/ml). The release of gastric glucagon was not affected by hyperglycemia alone but was reduced by about 40% when hyperglycemia was concomitant with an hyperinsulinemia within the physiological range. These observations support the concept that adequate concentrations of insulin are necessary in order for hyperglycemia to inhibit gastric glucagon secretion. Furthermore, it is suggested that the isolated perfused dog stomach might provide a unique tool permitting investigation of alpha-cell function in the absence of endogenously released insulin.
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PMID:Factors controlling gastric-glucagon release. 84 58

Hormonal and metabolic effects of a synthetic linear somatostatin were tested in insulin-dependent subjects submitted to an intravenous arginine infusion. Arginine alone induced a rise in plasma growth hormone (HGH) and glucagon (IRG) concentrations but did not affect the spontaneous diurnal decrease of plasma cortisol; blood glucose concentration rose while that of alanine decreased suggesting enhanced gluconeogenesis; concentrations of plasma free fatty acids (FFA) and 3-hydroxybutyrate decreased. Somatostatin, at three different dosages, markedly influenced these patterns: HGH response to arginine was suppressed by the lowest somatostatin dose; IRG response was progressively inhibited by increasing doses of somatostatin but never reached zero; cortisol level was not decreased but slightly increased by somatostatin. Substrate responses to arginine were also modified by somatostatin: alanine disappearance was impaired, this effect being dose-related; plasma FFA and 3-hydroxybutyrate concentrations showed a significant increase rather than decrease, consistent with somatostatin suppression of residual insulin secretion. Tolerance to somatostatin was good and no alteration of hemostasis was observed.
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PMID:Hormonal and metabolic effects of somatostatin in diabetic patients submitted to an i.v. arginine infusion. 87 Mar 53

To determine whether cyclic somatostatin (GH-RIH) interferes with glucose utilization and gluconeogenesis we studied levels of blood glucose (BG), immunoreactive insulin (IRI), immunoreactive glucagon (IRG) and of human growth hormone (GH) after iv glucose (330 mg/kg) and iv arginine (0.5 g/kg) in healthy subjects (n=8) and in maturity onset diabetics (n=8; fasting BG less than 200 mg/dl) both in the presence and in the absence of GH-RIH (500 microng/h iv). GH-RIH caused a reduction of glucose utilization in healthy subjects as shown by the decrease of the k-value from 2.08+/-0.22 (SE) % per min to 0.61+/-0.06 (SE) % per min (P less than 0.0005). No significant change of the glucose disappearance rate was observed in maturity onset diabetics by GH-RIH (kI=0.55+/-0.14 (SE) % per min; kII=0.42+/-0.03 (SE) % per min). The response of insulin to glucose was abolished by GH-RIH. The glucose induced suppression of IRG was in part significantly enhanced by GH-RIH in maturity onset diabetics (P less than 0.01). BG rises seen after iv arginine were increased by the administration of GH-RIH both in healthy subjects (P less than 0.001) and in maturity onset diabetics (P less than 0.05). Somatostatin abolished IRI and GH responses to arginine in both groups studied (P less than 0.001). IRG increases after arginine administration were diminished by GH-RIH in both groups (P less than 0.01). Our data demonstrate that GH-RIH impairs the iv carbohydrate tolerance in healthy subjects and facilities an increased hepatic glucose output upon administration of arginine both in controls and in maturity onset diabetics. We attribute the diabetogenic effect of somatostatin to suppression of IRI release rather than to changes in the IRG/IRI ratio in favor of IRG.
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PMID:The diabetogenic action of somatostatin in healthy subjects and in maturity onset diabetics. 87 May 15

True or 'pancreatic' glucagon-like immunoreactivity (GLI) was found in the plasma of a pancreatectomized patient. In contrast with the regulation of pancreatic GLI in normal controls, there was paradoxical release after oral glucose, no response to arginine or insulin-hypoglycaemia and somatostatin did not suppress its release, but tolbutamide did. Similar to controls, this pancreatic GLI appeared to be under adrenergic beta-receptor control. There was no apparent effect on blood glucose regulation despite marked changes in pancreatic GLI levels during the various manipulations. On polyacrylamide gel electrophoresis, pancreatic GLI from our patient's plasma eluted as two equivalent peaks: one with the glucagon marker and the other in a more cathodal position. We therefore suggest that, although the extra-pancreatic 'pancreatic' GLI in our patient's plasma has immunologic similarities with pancreatic glucagon, the responses to stimulation and suppression are quite different from those in controls and the biologic activity does not appear to be that of pancreatic glucagon.
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PMID:Pancreatic glucagon-like immunoreactivity in a pancreatectomized patient. 88 71


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