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 aim of the present study was to evaluate possible hemodynamic effects of somatostatin in insulin-dependent diabetic subjects. For this purpose, 7 insulin-requiring juvenile-onset diabetics were submitted to a short-term infusion of cyclic somatostatin (250 micrograms/h, over 2 h) or saline in randomized order. Somatostatin infusion resulted in a progressive and significant decrease in heart rate, stroke volume, cardiac index and velocity circumferential fiber; on the other hand, left ventricular ejection time was augmented by somatostatin. None of these effects was seen in the saline control study. We conclude that somatostatin exerts a negative inotropic effect in insulin-dependent diabetes.
Acta Diabetol Lat
PMID:Hemodynamic effects of somatostatin in insulin-dependent diabetic subjects. 4 64

This study was aimed at evaluating the effect of theophylline, a drug that increases the intracellular concentrations of cAMP by inhibiting phosphodiesterase activity, on somatostatin (SRIF)-mediated inhibition of insulin secretion in man. Acute insulin response (AIR) to i.v. glucose (mean change 3-10 min) was almost totally suppressed by SRIF (500 micrograms/h) and glucose utilization was reduced (p less than 0.0001). These SRIF-induced decreases failed to be eliminated by a concurrent infusion of theophylline (100 mg as a loading dose followed by a constant infusion of 5 mg/min). Theophylline alone resulted in a significant increase in both AIR (p less than 0.01) and glucose removal rates (p less than 0.05). Thus, our data disprove the involvement of the phosphodiesterase enzymes in the inhibitory action of SRIF on glucose-induced insulin secretion in man.
Acta Diabetol Lat
PMID:Somatostatin and insulin secretion in man. II. The effect of theophylline. 4 65

Plasma somatostatin immunoreactivity (SIR) was elevated 40-fold in an insulin-treated diabetic with disseminated pancreatic carcinoma. The diagnosis of somatostatinoma was supported by histological and ultrastructural similarities between metastatic cells and pancreatic D cells. Under acid conditions, 75% of the plasma SIR eluted as a 6000- to 7000-dalton protein and 25% as synthetic somatostatin (mol wt 1600), whereas the 20-fold elevated urine SIR consisted almost exclusively of the higher molecular weight fraction. The hypersomatostatinemia was associated with reduced basal and stimulated pancreatic hormone levels, which might reflect its involvement in the steatorrhea and diabetes, and its protection against ketoacidosis. Plasma SIR rose 50% upon insulin withdrawal and 10-fold after tolbutamide injection and fell 30% after diazoxide. It is concluded that an increase in plasma and urine SIR, the presence of a 6000- to 7000-dalton SIR fraction in plasma and urine, a reduction in basal and stimulated pancreatic hormone levels, and tolbutamide-induced somatostatin release can be diagnostic for a somatostatinoma. Streptozotocin reduced tumor volume, hypersomatostatinemia, and tolbutamide-induced somatostatin release, suggesting that this drug may be useful in the treatment of disseminated somatostatinoma.
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PMID:Plasma pancreatic hormone levels in a case of somatostatinoma: diagnostic and therapeutic implications. 15 32

The effects of somatostatin on tolbutamide-stimulated insulin release were studied in 4 patients with insulin-producing tumors of the pancreas and in 6 normal subjects. In contrast to its effective inhibition of insulin release in normal subjects, somatostatin, without exception, failed to inhibit tolbutamide-induced insulin release in the patients with pancreatic beta-cell tumors. This differential effect of somatostatin may prove useful in the diagnosis of insulin-producing tumors of the pancreas.
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PMID:Failure of somatostatin to inhibit tolbutamide-induced insulin secretion in patients with insulinomas: a possible diagnostic tool. 16 88

A number of enzymatic methods have been developed to prepare hepatocytes using collagenase and hyaluronidase. However, best cell preparations are obtained by using only low concentrations of collagenase and exposing the liver to the enzyme for a very short period of time. These isolated cells with intact cell membranes and large numbers of microvilli on the cell surface respond to hormones at physiological concentrations suggesting that these microvilli contain hormone receptors. In addition, high glycogen content is essential to maintain the in vivo metabolic characteristics of the hepatocytes suggesting that intracellular glycogen plays an important role in the hormonal regulation of metabolism in hepatocytes. Studies with glucagon and insulin on carbohydrate metabolism show that the molar ratios of these hormones control gluconeogenesis and glycogenolysis. Furthermore, in vitro addition of insulin stimulates glycogen synthesis and activates glycogen synthase. Insulin also stimulates protein synthesis in cells containing high glycogen and maintains more normal parallel strands of polyribosomes. Studies with isolated hepatocytes from diabetic, hypophysectomized and adrenalectomized animals show a reduced glucagon response to glycogenolysis. This lack of glucagon response was not due to reduction in glycogen levels. Other hormones such as somatostatin and parathyroid also give rise to alterations in carbohydrate metabolism in isolated hepatocytes.
Acta Diabetol Lat
PMID:Studies of hormonal regulation of metabolism using isolated hepatocytes. 19 66

Effects of somatostatin on fasting and arginine-or tolbutamide-stimulated insulin release were studied in four patients with insulinoma. Somatostatin (bolus or bolus + infusion) reduced fasting insulin values in all patients; insulin response to tolbutamide was partially reduced in two patients; somatostatin bolus impaired the insulin response to arginine. Fasting glucagon levels and glucagon response to arginine were also reduced by somatostatin. These results indicate the potential usefulness of somatostatin in the diagnosis of insulinoma even if its effect on insulin is only partial.
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PMID:Effects of somatostatin on insulin and glucagon in patients with insulinoma. 23 Oct 62

The effects of glucose, amino acids, pancreozymin-cholecystokinin, and tolbutamide upon the release of immunoreactive somatostatin (IRS) from the isolated perfused pancreas were studied. In seven experiments in which glucose was perfused either at a concentration of 100 or 350 mg/dl or at 25 mg/dl, IRS levels were significantly greater at the higher glucose concentrations. In three dose-response experiments in which the perfusing glucose concentration was increased at 30-min intervals from an initial concentration of 25 mg/dl to a final concentration of 300 mg/dl, progressive increases in IRS release were noted at glucose concentrations of 100 mg/dl and above. Perfusion of a 20 mM mixture of 10 amino acids also elicited a prompt and significant biphasic IRS rise in each of six experiments. In five experiments, 20 mM leucine evoked a similar response in mean IRS. Perfusion with 0.075 Ivy U/ml of pancreozymin-cholecystokinin, with or without the presence of a 1 mM 10-amino acid mixture, elicited a prompt rise in IRS with a pattern resembling that of insulin in a total of six experiments. Tolbutamide (0.75 mg/min) also stimulated IRS release in five of six challenges. The IRS responses to nutrients and to pancreozymin and their similarity to the insulin responses raise the possibility that, like insulin, pancreatic somatostatin may have an endocrine role related to nutrient homeostasis.
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PMID:Release of immunoreactive somatostatin from the pancreas in response to glucose, amino acids, pancreozymin-cholecystokinin, and tolbutamide. 33 May 67

1. Investigation of the ionic requirements of the in vitro insulin release system, which consists of cod islet plasma membrane and rabbit islet granules incubated at pH 6.5, showed that the presence of Ca(2+) was obligatory for the system to operate.2. Glucose-initiated insulin release was as effective in the presence of beta-gamma-methylene ATP, as it was in the presence of ATP. This analogue of ATP is a substrate neither for adenylate cyclase nor for any known animal membrane proteases. The effect of ATP on glucose mediated release is allosteric.3. Glucose (16 mM)-initiated insulin release was slower than that induced by glucose-6-phosphate (4 mM); 150 and 120 sec, respectively.4. The lag found with glucose-mediated insulin release was dependent upon glucose concentration. The lower the glucose concentration, the longer the lag. With 1 mM glucose the lag extended to 30 min.5. Once insulin release was initiated, the rate and amount of insulin release was independent of the glucose concentration.6. Pre-incubation of membranes with Ca(2+), glucose and ATP prior to the addition of granules, abolished the extended lag that had been obtained with 1 mM glucose. Events in the plasma membrane are the major contributor to the generation of the extended lag.7. The glucose analogue 5'thio-D-glucose, although not able to release insulin, was shown to compete with glucose for the glucoreceptor. By increasing the ratio of analogue to glucose the lag time increased. Thus, the lag time is dependent upon the ;effective' external glucose concentration.8. The max. amount of insulin released by 4 ng of membrane in the presence of glucose (16 mM) was 300 ng. The fact that membranes became refractory to glucose after this max. amount of insulin was released showed that recycling of release sites was not taking place in vitro and that granule: granule interactions were not occurring.9. The 120 sec lag before glucose-6-phosphate-initiated release was independent of glucose-6-phosphate concentration. The rate of insulin release with glucose-6-phosphate was concentration dependent.10. Glucose-6-phosphate did not cause further insulin release from a membrane that had released the max. amount of insulin it was capable of in the presence of glucose. The addition of tolbutamide (10 mM) to such a membrane did cause insulin release. This suggests that glucose and glucose-6-phosphate share a final common pathway.11. Adrenaline and somatostatin did not inhibit glucose-mediated insulin release.
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PMID:An in vitro system for studying insulin release: effects of glucose and glucose-6-phosphate. 33 48

Pharmacodynamic characteristics of pentoxyfylline (BL 191) related to insulin secretion by the isolated perfused rat pancreas are studied. The results obtained show that: 1) BL 191 (5 mM) is capable of stimulating insulin secretion, even in the presence of another stimulator; 2) BL 191 increases both phases of the secretion produced by constant arginine 20 mM/glucose 5 mM perfusion; 3) BL 191 significantly increases and turns biphasic the monophasic insulin secretion pattern produced by 1 microgram/ml glibenclamide; 4) the effects mentioned in points 2) and 3) are inhibited if the phosphodiesterase activator imidazole (300 mg/100 ml) is present in the perfusion medium; 5) the phosphodiesterase inhibitor theophylline has the same effects as BL 191, except for its inability to stimulate insulin release in the absence of another stimulator; 6) somatostatin (100 ng/ml) significantly inhibits insulin secretion produced by arginine/glucose or glibenclamide, as well as by arginine, glucose plus theophylline or BL 191, and by glibenclamide plus theophylline or BL 191, in both cases the inhibitory effect of somatostatin is reduced by the presence of BL 191 or theophylline.
Acta Diabetol Lat
PMID:The influence of pentoxyfylline [1-(5-oxohexyl-) 3,7-dimethylxanthine] (BL 191) on the insulin secretion induced by glibenclamide and by arginine/glucose in the perfused pancreas. 41 15

The aim of this study was to compare the metabolic and hormonal effects of somatostatin to those of propranolol, a beta-adrenergic blocking agent known to reduce basal insulin secretion. For this purpose, 6 normal subjects received somatostatin (4 microgram/min) per 60 min and 6 subjects were infused with propranolol (0.08 mg/min). Somatostatin resulted in a significant decrease of basal insulin (p less than 0.05) and glucagon (p less than 0.01) and raised plasma FFA levels from a mean basal value of 417 +/- 24 muEq/1 (x +/- SEM) to 600 +/- 46 muEq/1 at 60 min (p less than 0.01). Propranolol significantly decreased basal insulin (p less than 0.05) and glucagon (p less than 0.05); FFA levels rose slightly at the end of propranolol administration (p less than 0.05). The levels of FFA which were significantly higher (p less than 0.025) during somatostatin as compared to those observed during propranolol, seem to suggest a role for this tetradecapeptide in lipid metabolism independent of its inhibiting action on islet hormone release.
Acta Diabetol Lat
PMID:A comparative study of metabolic and hormonal responses to somatostatin and propranolol in man. 45 22


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