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)

This study was performed in order to investigate the effect of a 12-h infusion of the somatostatin selective analog D-Trp8, D-Cys14 Serono, (SRIF-A), on insuli requirement and C-peptide (CP), growth hormone (GH) and glucagon (IRG) levels in 6 insulin-dependent diabetics submitted to 60-h artificial pancreas (Biostator Miles) metabolic control from 2000 of the first day to 0800 of the fourth day. Meals were given at 1200 and 1700 of the second and third day. Before meals and 1-2 h after meals, plasma levels of CP, GH and IRG were measured. The two 12-h periods (midday-midnight) with and without continuous SRIF-A 12-h infusion (40 microgram/h) were considered. The SRIF-A infusion caused a 20% reduction in insulin requirement (p < 0.05) and a slight but significant reduction of GH levels (p < 0.05). CP and IRG were unaffected.
Acta Diabetol Lat
PMID:Effect of a somatostatin analog on insulin requirement and hormone levels in 6 insulin-dependent juvenile-onset diabetics subjected to artificial pancreas. 610 42

To study the possible role of the secretion vesicle inligant-receptor interaction, somatostatin binding was measured in islets in the presence of various substances known to promote secretion vesicle migration and fusion with the plasma membrane and insulin release. Rat islets were incubated with glucose, 30 and 300 mg/dl, for 60 min. After inculation, somatostatin binding was measured. In islets preincubated with glucose, 300 mg/dl, somatostatin binding was increased 250% when compared with glucose, 30 mg/dl (P < 0.001). Concomitant with enhanced somatostatin binding, insulin secretion was increased. Galactose, 300 mg/dl, did not stimulate insulin release, and somatostatin binding was unchanged from control levels. The increase in somatostatin binding with glucose was accounted for by a 186% increase in receptor concentration with no change in receptor affinity. Tolbutamide increased somatostatin binding by more than twofold, accompanied by a similar increase in insulin release. Secretion vesicles isolated from the islet exhibited somatostatin binding. We conclude that, first, somatostatin binding is increased concomitantly with the migration and fusion of the secretion vesicle with the plasma membrane and/or the release of insulin; second, enhanced somatostatin binding occurs as a consequence of an increased receptor concentration; and third, augmented somatostatin binding occurring with hormone release may provide a critical constraint in the regulation of secretory events.
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PMID:Role of insulin secretagogues in the regulation of somatostatin binding by isolated rat islets. 610 33

The effects of HB 699, a non-sulphonyl urea acyl-amino-alcyl benzoic acid derivative, were studied in unanesthetized dogs. Changes in blood glucose and plasma insulin, glucagon, pancreatic polypeptide and somatostatin were measured after a single intravenous injection. HB 699 caused hypoglycaemia and stimulated insulin secretion in a dose-dependent manner. The effects of HB 699 (40 mg/kg) on pancreatic hormone secretion were compared to those of tolbutamide give at a dose (12 mg/kg) which induced a similar maximal hypoglycaemia. Both drugs caused a similar increase in insulin release (180 +/- 32% for tolbutamide and 240 +/- 41% for HB 699) lasting for approximately 1 hour. Despite hypoglycaemia, plasma glucagon concentrations were unaltered by either substance. HB 699 caused a marked increase in the secretion of pancreatic polypeptide (220 +/- 60% at 30 min) for up to 2 hours, whereas tolbutamide caused no significant change in plasma pancreatic polypeptide levels. In contrast, while tolbutamide caused a significant (45 +/- 12%) but short-lived increase in plasma somatostatin concentrations, HB 699 had no significant effect.
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PMID:Effect of a new hypoglycaemic agent (HB 699) on the in vivo secretion of pancreatic hormones in the dog. 611 83

An animal model of diabetes mellitus has been developed in which neonatal rats are injected with streptozotocin at 2 days of age. After transient hyperglycemia followed by near normal glycemia, these animals develop nonketotic diabetes at about 6 wk of age that does not require insulin treatment. Secretion form the endocrine pancreas of 6-15-wk-old rats was evaluated with the isolated, perfused pancreas technique. Insulin secretion responded very poorly to high perfusate glucose concentrations, but in the presence of theophylline this meager response was enhanced. In contrast, arginine elicited an insulin response comparable to that of the control rats. Isoproterenol stimulated insulin secretion more in the diabetic model than in the controls, and tolbutamide failed to evoke insulin secretion. Glucagon secretion in response to arginine and isoproterenol was similar in both groups, but was suppressed less efficiently be glucose in the model than in controls. Evidence for enhanced basal secretion of somatostatin was also found. Thus, these hyperglycemic rats have a selective defect in glucose-stimulated insulin secretion with preservation of responses to other agents. In addition, abnormalities in the secretion of glucagon and somatostatin have been found.
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PMID:Islet secretion in a new experimental model for non-insulin-dependent diabetes. 611 5

We have studied the effects of starvation and of obesity on somatostatin, insulin, and glucagon release from an isolated perfused organ system in fed and 3- and 5-day fasted Holtzman rats and in obese (fa/fa) and lean (Fa/?) Zucker rats. Fasting for 3 days significantly decreased basal (-71%) and amino acid-stimulated (-62%) somatostatin output. After 5 days of starvation, there was a significant increase over the 3-day level in somatostatin output stimulated by amino acid plus glucose (+540%) and by amino acids plus tolbutamide (+238%). Three and five days of starvation severely depressed insulin output while having no statistically significant effects on glucagon secretion. Somatostatin output from obese Zucker rats was significantly greater than that from lean controls in response to amino acids (41.2 +/- 13.2 vs. 16.3 +/- 10.3 ng/25 min, P less than 0.05). Insulin output was greatly increased from obese compared to lean Zucker rats, whereas there were no statistically significant differences in glucagon output. These data show that fasting decreases and obesity increases both somatostatin and insulin release. They suggest that altered stimulation by nutrients was primarily responsible for changes in somatostatin and insulin release observed in starving and obese rats.
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PMID:Effects of starvation and obesity on somatostatin, insulin, and glucagon release from an isolated perfused organ system. 611 33

An argyrophilic fourth cell type in fetal and adult rat pancreatic islets can be identifed by using a modification of the Grimelius silver statin. This cell is much more abundant in the fetal pancreas than in the adult. By employing the modified silver technique followed by restaining with the indirect immunofluorescent procedure for somatostatin, the content of this argyrophilic fourth cell was studied further. Comparison of these histochemical studies demonstrated that somatostatin was not located in the fourth cell of either the adult or fetal rat pancreas. These results indicate that the D-cell and the fourth cell type are not the same cell. Thus far the only product associated with this argyrophilic cell is pancreatic polypeptide. As a result this cell probably represents the PP-cell of the Wiesbaden classification.
Acta Diabetol Lat
PMID:Further evidence for an argyrophilic fourth cell type in the pancreatic islet of the rat. 611 1

Mice treated for 4 days with tolbutamide displayed decreased serum glucose values with a concomitant decrease of their islet insulin content. Mouse islets cultured for 1 week at a low (3 mM) or a high (28 mM) glucose concentration contained less insulin than non-cultured islets and islets cultured at a medium (11 mM) glucose concentration. All groups of cultured islets contained more glucagon than non-cultured islets. The somatostatin content of high- and medium-glucose cultured islets was higher than that of freshly isolated islets.
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PMID:Hormone content of mouse pancreatic islets subjected to different in vivo and in vitro functional demands. 611 26

The effects of glucose alone, combinations of glucose with arginine or tolbutamide and either arginine or tolbutamide alone, on somatostatin, insulin, and glucagon secretion were investigated using the isolated perfused rat pancreas. When glucose alone was raised in graded increments at 15-min intervals from an initial concentration of 0 mM to a maximum of 16.7 mM, somatostatin as well as insulin in the perfusate increased with the glucose, while glucagon decreased. The similarity of the glucose stimulated somatostatin and insulin release was especially evident when the perfusate glucose was increased from an initial dose of 4.4 mM rather than 0 mM to 8.8 mM or 16.7 mM. In addition, glucose at concentrations varying from 4.4 mM to 11 mM dose-dependently enhanced arginine-induced somatostatin and insulin release and suppressed glucagon release dose-dependently as before. Arginine in the absence of glucose was not capable of stimulating somatostatin secretion whereas tolbutamide, in contrast, was capable of stimulating somatostatin secretion even in the absence of glucose.
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PMID:Glucose regulation of arginine-induced pancreatic somatostatin release from the isolated perfused rat pancreas. 612 38

The effect of tolbutamide on somatostatin release from the isolated perfused stomach was investigated in both normal and streptozotocin-diabetic rats. Tolbutamide (10, 100, and 1000 microgram/ml) evoked a significant and dose-dependent increase in gastric somatostatin release. The tolbutamide (100 microgram/ml)-induced gastric somatostatin secretion was not influenced by differences in glucose concentration (1.5, 5.5, and 16.5 mM) throughout the perfusion period. Tolbutamide (100 microgram/ml)-induced gastric somatostatin release in streptozotocin-diabetic rats was significantly higher than in normal rats. Thus, tolbutamide is a potent secretagogue for gastric somatostatin secretion, and this effect is more prominent in diabetic animals.
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PMID:Tolbutamide stimulates gastric somatostatin release from isolated perfused rat stomach. 613 15

Five cases of somatostatinoma are reported, four being primarily located in the pancreas and one in the duodenum. The diagnosis was based upon the histological and immunochemical characteristics of tumoral and metastatic tissue. A marked clinical heterogeneity was noted: one patient presented with gallstones, steatorrhea, and diabetes, two patients suffered from severe hypoglycemic attacks, and two cases were admitted for obstructive jaundice. This varying symptomatology was related to differences in the circulating levels of biologically active somatostatin and to a variable cellular composition of the tumor. In all cases, a basal and/or tolbutamide-induced hypersomatostatinemia was measured. It is concluded that the clinical and hormonal features of the earlier defined somatostatinoma syndrome are no requisite for the diagnosis of somatostatinoma; the analysis of plasma somatostatin immunoreactivity might lead to a higher detection rate of this endocrine tumor.
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PMID:Five cases of somatostatinoma: clinical heterogeneity and diagnostic usefulness of basal and tolbutamide-induced hypersomatostatinemia. 613 27


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