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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect os somatostatin (SS) and of its analogs D Trp 8-SS and Asn 5-SS was studied upon the external pancreatic secretion of the Rat after stimulation by 2 deoxy-D-glucose. The secretion of sodium and bicarbonate was similarly inhibited by all four peptides. The analog D Trp 8-SS was more effective in inhibiting pancreatic protein excretion.
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PMID:[Action of somatostatin and 3 analogs on external pancreatic secretion in the rat]. 10 39

Glucose-induced insulin secretion is enhanced by a preceeding glucose stimulus. The characteristics of this action of glucose were investigated in perfused pancreas and collagenase-isolated islets of Langerhans. A 20- to 30-min pulse of 27.7 mM glucose enhanced both the first and second phase of insulin release in response to a second glucose stimulus by 76-201%. This enhancement was apparent as an augmented maximal insulin release response to glucose. The effect of priming with glucose was seen irrespective of whether the pancreatic tissue was obtained from fed or fasted rats. Separating the two pulses of hexose by a 60-min time interval of exposure to 3.3 mM glucose did not abolish the potentiation of the second pulse. Omission of Ca(++) as well as the inclusion of somatostatin or mannoheptulose during the first pulse abolished insulin secretion during this time period; however, only the inclusion of mannoheptulose deleted the potentiation of the second pulse. d-Glyceraldehyde, but not pyruvate, d-galactose, or 3-isobutyl-1-methylxanthine, could substitute for glucose in inducing potentiation. In islets labeled with [2-(3)H]adenine, the [(3)H]cyclic AMP response to glucose was increased by 35% when measured after 1 min, but was increased only marginally after 2-10 min of stimulation with a second pulse of glucose. The production of (3)H(2)O from glucose was not affected by glucose priming. It is concluded that (a) the induction of the glucose-induced, time-dependent potentiation described here is dependent on glucose metabolism but not on stimulation of cyclic AMP, calcium fluxes, or insulin release per se; (b) the mechanisms that mediate the pancreatic "memory" for glucose are unknown but do not seem to involve to a major extent an increased activity of the adenylate cyclase-cyclic AMP system of the beta-cell; (c) the evidence presented supports the hypothesis of a dual role of glucose for insulin release.
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PMID:Immediate and time-dependent effects of glucose on insulin release from rat pancreatic tissue. Evidence for different mechanisms of action. 20 21

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

Oral carbohydrate tolerance tests with xylose, galactose and lactose were performed. After an interval of at least 24 h the same tests were repeated following an i.v. bolus and during infusion of somatostatin. Somatostatin does not influence xylose absorption. However, absorption of galactose and lactose is significantly reduced (p less than 0.01/0.008) during somatostatin infusion. On the other hand, serum levels of galactose remain unchanged despite administration of somatostatin, when galactose is given parenterally. The results support the assumption that the absorption process in small intestine is affected by somatostatin. Possible effects of somatostatin on hormones regulating the intestinal absorption and on energy-depending carrier mechanisms are discussed.
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PMID:Influence of somatostatin on carbohydrate absorption in human small intestine. 43 79

Somatostatin inhibits in a dose-dependent manner the glucagon secretion in the presence of up to 5 mM glucose, whereas the suppressed glucagon release in the presence of greater than or equal to 10 mM glucose, 10 mM glyceraldehyde, 30 mM fructose or 30 mM mannose is characterized by an increase of hormone release under the influence of somatostatin.
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PMID:Modulation of the hexose induced suppression of glucagon secretion by somatostatin on isolated pancreatic rat islets. 78 24

By means of a glucose-controlled insulin- and glucose-infusion system (GCIGIS) we examined the effect of somatostatin on insulin and glucose requirements following meals or oral glucose loads in juvenile diabetics. In six of seven patients the insulin requirement with somatostatin was remarkably reduced to between 38 per cent and 79 per cent of that of otherwise identical control experiments. No reduction could be found in the seventh case, fed only 575 kcal. In all cases we observed an increase in dextrose demanded from the GCIGIS ranging between 28 per cent and 192 per cent of the control amounts. In addition, a lowering and smoothing of postprandial blood glucose curves caused by somatostatin application was a general finding. It seems to us most likely that the well-known suppression of the secretion of growth hormone and glucagon, both insulin antagonists, is responsible for the antidiabetic action of somatostatin.
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PMID:Antidiabetic action of somatostatin--assessed by the artificial pancreas. 110 69

This study examines the effects of donor age on exogenous somatostatin inhibition of insulin secretion stimulated by 10 mM D-glyceraldehyde and by 20 mM beta-D-glucose in isolated perfused rat pancreas. Both 6 and 30 nM synthetic somatostatin-14 affect both glyceraldehyde- and glucose-stimulated insulin secretion to a greater degree in pancreases from old animals (24-27 months) than in those from young (2-5 months). We conclude that an increased sensitivity to inhibitory actions of somatostatin during aging, observed in pituitary tissues in vitro, occurs in pancreatic tissues as well and may constitute a general phenomenon in tissues subject to somatostatin inhibition.
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PMID:Aging enhances inhibitory action of somatostatin in rat pancreas. 134 43

Two studies were performed to determine the importance of endogenous somatostatin (SS) in regulating human TSH secretion. In the first, healthy adult males were studied in random order on two occasions a week apart. They were infused with either saline to maintain euglycaemia, or 10% dextrose to raise blood glucose concentration by at least 3 mmol/L within 10 minutes, and cause hypothalamic SS release. Fifteen minutes after the infusions were commenced, 200 micrograms of TRH was injected intravenously and TSH release was followed for the next 75 minutes. In the second study, persons with elevations of TSH to between 3 and 12 mU/L were also infused with either saline or 10% dextrose. Infusions were continued for 1 hour and the TSH secreted was measured over this time period. There was no significant difference between the euglycaemic or hyperglycaemic studies in TRH-induced TSH secretion, either as areas under the curve, or as mean values at individual times. Mean TSH peaks were seen in both groups at 25 minutes post-TRH. Mean peak values were 8.11 +/- 0.97 mU/L (mean +/- SEM) in the euglycaemic group, and 7.94 +/- 1.18 mU/L in the hyperglycaemic group. Mean area under the curve was 396.3 +/- 53.2 mU/L/75 mins (SEM) for the euglycaemic study and 385.1 +/- 59.5 mU/L/75 mins (SEM) for the hyperglycaemic group. In the infusion study in the persons with mild hypothyroidism, there was no difference in TSH concentration between the two infusion regimes. These results show that in acute studies, hyperglycaemia does not inhibit human TSH release, despite the likelihood of hypothalamic-pituitary SS concentration being increased.
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PMID:The effect of endogenous somatostatin upon human thyrotrophin (TSH) secretion. 134 94

A 15 year old girl with a family history of type 1 multiple endocrine adenomatosis presented with reversible neurological disturbances, hypoglycaemia and hyperinsulinaemia. Initial radiology was normal, but portal venous sampling suggested an insulinoma in the tail of the pancreas which was removed with conservation of the spleen. Hypoglycaemia persisted despite high doses of diazoxide and intravenous dextrose. A second laparotomy revealed a pancreatic endocrine tumour and sub-total pancreatectomy was performed. Histology revealed islet cell microadenomatosis. Hypoglycaemia persisted despite treatment with somatostatin analogues and 40% intravenous dextrose was required to maintain normoglycaemia. A possible lesion near the splenic hilum on computed tomographic scan was reported as a splenunculus although further peripheral, hepatic and portal venous sampling suggested hepatic or systemic lesions. A positron emission scan and selective visceral angiography suggested a lesion in the left upper quadrant. Acute lactic acidosis, rhabdomyolysis and renal failure supervened. Post mortem revealed the putative 'splenunculus' to be a residual insulinoma, whilst the splenic vein was thrombosed, accounting in part for discrepant venous sampling data. Hyperinsulinaemia in type 1 multiple endocrine adenomatosis may require more aggressive surgical and hormonal intervention than when dealing with solitary insulinomas. Insulinomas may mimic developmental abnormalities on computed tomographic scanning.
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PMID:Difficulties in localization and treatment of insulinomas in type 1 multiple endocrine adenomatosis (MEA). 135 Mar 44

The distribution of binding by the isolectin I-B4 from Griffonia simplicifolia in the rat trigeminal system has been investigated. This lectin binds to a sub-population of small-diameter trigeminal ganglion neurons. Double-labelling studies revealed that this lectin bound to all the trigeminal ganglion neurons containing somatostatin, whereas it bound to less than 25% of those containing calcitonin gene-related peptide or substance P. In the brainstem this lectin gave terminal-like staining in only the sub-nucleus caudalis of the trigeminal nuclei. In this nucleus, staining was most dense in the inner part of lamina II. Morphometric studies suggest that this lectin and that from the soybean recognize the same population of cells. The relationship of this data to those obtained in other studies using markers binding to glycoconjugates with a terminal alpha-galactose is discussed.
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PMID:The distribution of binding by isolectin I-B4 from Griffonia simplicifolia in the trigeminal ganglion and brainstem trigeminal nuclei in the rat. 137 53


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