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)

Juvenile diabetic patients were studied 60-72 hours after insulin withdrawal when moderate ketoacidosis had developed. Somatostatin infusion for 4 hours in five patients resulted in almost complete suppression of plasma pancreatic glucagon and growth hormone, a fall in plasma-cyclic-adenosine-monophosphate (A.M.P.) concentrations, and a large fall in plasma-glucose concentration. After infusion plasma concentrations of these substances rose again. Blood-ketone-bodies, plasma-free-fatty-acids (F.F.A.), and plasma glycerol concentrations, however, did not decrease appreciably with somatostatin administration. In three patients 2 to 3 h somatostatin infusions were twice superimposed upon a continuous 9-5 h insulin infusion (1 unit/h). An insulin effect was noticeable within 30 minutes, with pronounced falls in the concentrations of plasma glucose, pancreatic glucagon, F.F.A., and blood-ketone-bodies. There was no significant change in these patterns when somatostatin was administered or withdrawn. These results do not indicate that somatostatin infusion would be useful in the treatment of manifest diabetic ketoacidosis.
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PMID:Failure of somatostatin to correct manifest diabetic ketoacidosis. 5 30

Infusion of somatostatin, an inhibitor of glucagon secretion, in insulin-dependent diabetics resulted in a 75-100% reduction in the blood-glucose rise after oral glucose administration, but did not improve intravenous glucose tolerance. Somatostatin reduced blood-xylose levels by 50-90% after ingestion of this pentose and delayed the peak increment in blood-xylose by 1-2 h. Similar effects on blood-xylose levels and a 30% reduction in splanchnic blood-flow were observed in normal subjects during infusion of somatostatin. Glucagon administration (3 ng per kg per min) or intraduodenal administration of xylose did not reverse somatostatin's effect on xylose tolerance. Somatostatin reduces postprandial hyperglycaemia in diabetes primarily by decreasing and/or delaying carbohydrate absorption rather than enhancing carbohydrate disposal. This effect may be mediated, in part, but a reduction in splanchnic blood-flow. These findings indicate that postprandial hyperglycaemia in diabetes is due primarily to insulin deficiency rather than glucagon excess.
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PMID:Influence of somatostatin on carbohydrate disposal and absorption in diabetes mellitus. 6 40

Extracts of homogenates of rat, mouse, rabbit, and human submaxillary salivary glands contain a significant quantity of a material with glucagon-like immunoreactivity. Fractionation of this material on columns of Sephadex G-100 reveals a single peak immediately following a gamma globulin marker but in advance of a rat growth hormone marker, crystalline amylase, and isotopically labeled porcine insulin and glucagon. This material, which is urea stable, shows identical immunoassay dilution curves when measured with the highly specific K-30 glucagon antiserum. Study of paired glands in vitro shows that low concentrations of glucose stimulate and high concentrations of glucose suppress release of this material. Arginine promotes brisk release in vitro. Somatostatin does not influence arginine-stimulated secretion and insignificantly suppresses basal release in vitro. These findings lend support to previous speculations that the salivary glands may possess endocrine as well as exocrine functions. Salivary gland glucagon may also be the source of circulating glucagon recently reported in pancreatectomized and eviscerated rats.
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PMID:Salivary gland hyperglycemic factor: an extrapancreatic source of glucagon-like material. 6 92

The first case of a tumour producing somatostatin-like immunoreactivity and bioactivity is presented. The pancreatic tumour was composed of cells indistinguishable from islet D cells. Radioimmunoassay of blood-samples obtained by tumour-vein catheterisation revealed very high levels of somatostatin immunoreactivity. On gel chromatography tumour extracts were found to contain at least 4 different immunoreactive components, one of which eluted in the position of synthetic somatostatin. Extracts from the tumour were potent in inhibiting insulin and glucagon secretion from isolated perfused porcine pancreas. Clinical abnormalities included hypochlorhydria, steatorrhoea, and diabetic glucose tolerance. Conceivably some of these abnormalities may be related to somatostatin hypersecretion from the pancreatic tumour.
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PMID:Pancreatic somatostatinoma. Clinical features and physiological implications. 6 72

The hyperglycemic activities of epinephrine (EPI) and isoproterenol (ISO) in baboons correlated with their ability to increase plasma glucagon (IRG) levels relative to insulin (IRI). EPI inhibited IRI release and produced greater increases in plasma glucose and IRG than did ISO. ISO increased plasma IRI levels more than IRG. Infusion of somatostatin blocked IRG release and inhibited hyperglycemic responses to EPI by approximately 50%. These findings indicate that, as in man, IRG release contributes significantly to the hyperglycemic effects of catecholamines in baboons. The baboon thus appears to be a suitable model for predicting effects of drugs on glucose homeostasis in humans.
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PMID:Role of glucagon in the hyperglycemic response to catecholamines in fasted baboons. 9 54

For more than half a century the management of hyperglycemia in diabetes mellitus has included rigid diets and intermittent subcutaneous insulin administration. These methods have been totally unsuccessful in restoring glucose homeostasis to normal in most diabetic patients. This review focuses on techniques that offer promise as alternatives or adjuncts to the current modalities of treatment. Specific areas discussed include pancreatic transplantation, islet cell transplantation, artificial beta cell devices, and the glucagon-suppressing agent somatostatin. Although many of these show promise for the future, a cure for the metabolic abnormalities of diabetes is not imminent.
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PMID:Treatment of diabetes mellitus: the future. 10 34

The effect of a sulfonylurea, glibenclamide, on the release of insulin, glucagon, and somatostatin was studied in the isolated perfused rat pancreas. At glucose concentrations of 1.1 mM or less, the drug stimulated somatostatin release, whereas glucagon release, after 2-3 min of increase, was markedly inhibited. Insulin release was moderately stimulated, and maximal release occurred relatively late. A moderate glucose load (6.7 mM) inhibited glibenclamide-induced release of somatostatin, whereas the two in combination exerted an additive action on insulin release. Greater glucose loads, which by themselves would stimulate somatostatin release, only marginally suppressed glibenclamide-induced somatostatin release. The insulinogenic effect of these glucose levels was not modified by glibenclamide. Glibenclamide may thus stimulate both the alpha and beta as well as delta cells of the pancreas, depending on glucose concentration. We suggest a paracrine (local) interaction of somatostatin with the alpha and beta cells, which has an important role in the kinetics of insulin and glucagon release induced by sulfonylureas.
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PMID:Effect of glucose/sulfonylurea interaction on release of insulin, glucagon, and somatostatin from isolated perfused rat pancreas. 11 58

Growth hormone regulation was studied in 10 patients with Huntington's disease after intravenous administration of arginine. In 20 control subjects arginine infusion resulted in a rise of plasma growth hormone levels from a mean baseline value of 3.2+/-0.6 ng/ml to a peak level of 17.6+/-2.7 ng/ml at 60 min. Growth hormone rise in the majority of patients with Huntington's disease was clearly intact and significantly greater than normal in magnitude, increasing from the baseline level of 2.6+/-0.5 ng/ml to a peak level of 28.3+/-3.7 ng/ml at 60 min (P = less than 0.05). Carbohydrate tolerance of these patients was previously examined, and 4 with normal glucose tolerance and normal insulin responses to arginine infusion had growth hormone levels significantly higher than controls at 30 min. Six patients with impaired carbohydrate tolerance and exaggerated insulin responses to arginine had significantly higher growth hormone responses at 30 min and also at 60 min. Neuronal degeneration of several hypothalamic nuclei has been reported in Huntington's disease. The observations that growth hormone responds in an exaggerated fashion to stimulation by arginine infusion or falling glucose levels as previously described may be explained by intrahypothalamic dysfunction such as impairment of somatostatin secretion.
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PMID:Exaggerated growth hormone response to arginine infusion in Huntington's disease. 12 87

Shifts in the distribution of the monovalent cations Na+ and K+ between the extra- and intracellular space seem to be important for the secretory response of the beta-cell. An attempt was therefore made to study the enzyme responsible for monovalent cation transport, the (NaK)-activated ATPase. In the presence of NaN3 as inhibitor of the mitochondrial Mg-ATPase, a NaK-ATPase with a specific activity of 72 mU X mg protein-1 could be demonstrated in crude membrane preparations of rat pancreatic islets. The enzyme, which was inactive in the absence of Mg++, needed both Na+ and K+ for activation and was inhibited by ouabain and PCMB. The main part of the NaK-ATPase was localized in the microsomal fraction. Glucose, sulphonylureas, somatostatin and diazoxide were without effect on NaK-ATPase.
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PMID:NaK-ATPase in rat pancreatic islets. 14 87

The endocrine pancreatic tissue from patients with severe primary chronic pancreatitis (n=6). secondary chronic pancreatitis due to duct obstruction by carcinoma (n=6) and non-diabetic, non-pancreatitic controls (n=4) was studied qualitatively and quantitatively using specific immunocytochemistry and electron microscopy. Grouping of variously sized islets in the sclerotic tissue (sclerosis islets), islet neoformation by ductuloinsular proliferation, and intrainsular fibrosis were the main qualitative findings. Immunocytochemical quantitation of the distribution of insulin (B), glucagon (A), somatostatin (D) and pancreatic polypeptide (PP) producing cells revealed a significant relative increase in the number of A cells and a decrease in the number of B cells of the sclerosis islets in primary chronic pancreatitis ((B-44.1+/-9.3%:A-38.3+/-2.4%:D-8.6+/-5.1%:PP-4.6+/-4.1%) as well as in secondary chronic pancreatitis B-38.0+/-14.3%:A-38.4+/-19.0%:D-9.1+/-5.8%:PP-14.5+/-23.4%) compared with controls (B-71.1+/-8.1%:A-24.3+/-5.5%:D-8.0+/-2.8%:PP-0.5+/-0.4%). The number of PP cells was significantly increased in primary chronic pancreatitis only. It is suggested that scarring of the exocrine pancreas affects islet composition, probably by impairment of the local circulation and of glucose diffusion, thus leading to reduction of the number and glucose sensitivity of B cells. The hyperplasia of A and PP cells appears to be a secondary phenomenon due to the loss of B cells.
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PMID:The endocrine pancreas in chronic pancreatitis. Immunocytochemical and ultrastructural studies. 14 59


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