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)

In isolated perfused rat pancreases, the alpha-anomer of D-glucose is more potent than beta-D-glucose not solely in stimulating insulin release and suppressing glucagon output, but also in causing somatostatin secretion.
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PMID:Anomeric specificity of glucose-induced somatostatin secretion. 289 61

Brush border membrane vesicles (BBMV) and basolateral membrane vesicles (BLMV) were simultaneously prepared from surgically resected pieces of morphologically intact human duodenum with a modified Percoll gradient centrifugation method. Alkaline phosphatase was enriched 20-fold in BBMV, whereas (Na+ + K+)-stimulated adenosine triphosphatase was enriched 15-fold in BLMV. BBMV and BLMV were preincubated with 3 microM synthetic somatostatin-14 or 3 microM SMS 201-995 for 10 min at 5 degrees C. In BBMV calcium, sodium, D-glucose, L-alanine, and D-mannitol uptake was unaffected by somatostatin-14 and SMS 201-995. In BLMV we found two Ca++ transport systems: Na+/Ca++ exchange and ATP-driven Ca++ transport. Somatostatin-14 had no effect on either of the two transport mechanisms. SMS 201-995 had no effect on Na+/Ca++ exchange but significantly inhibited basolateral ATP-dependent Ca++ transport (-40% +/- 5%, p less than 0.005).
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PMID:Effect of the somatostatin analogue SMS 201-995 on ATP-dependent calcium transport of basolateral vesicles from human duodenum. 289 47

We have evaluated the potential of the clonal insulin-secretory cell line HIT-T15 as a model system for investigating stimulus-secretion coupling in pancreatic B cells. In contrast to other cell lines, HIT cell insulin secretion was consistently stimulated 2- to 3-fold by D-glucose. The maximally effective concentration of glucose was 10 mmol/l; between 2 and 10 mmol/l glucose the increase in insulin release was paralleled by an increased rate of glucose oxidation. The main characteristics of glucose-stimulated insulin release by HIT cells were essentially similar to those of normal islets. Thus, the response was specific for metabolizable sugars (D-mannose and D-glyceraldehyde stimulated insulin release but L-glucose and D-galactose were ineffective); markedly dependent on extracellular Ca2+ concentration; potentiated by forskolin, glucagon, acetylcholine and 12-O-tetradecanoyl phorbol 13-acetate; inhibited by adrenaline or somatostatin; showed a biphasic pattern of release in perifusion experiments, with both phases being potentiated by forskolin. The secretory response of the HIT cells to amino acids was also similar to that of normal islets. Thus, L-leucine and its deamination product 2-ketoisocaproate were effective stimuli, whereas L-isoleucine and L-glutamine were ineffective. Insulin release from HIT cells could also be evoked by the sulphonylureas glibenclamide and tolbutamide and by an increase in concentration of extracellular K+ to 40 mmol/l. The content of cyclic AMP in HIT cells was increased modestly by glucose but not by an increase in extracellular K+. Forskolin elicited a 4-fold increase in cyclic AMP content. We conclude that HIT cells retain the essential features of the insulin secretory response of normal B cells and represent an important tool for further biochemical characterization of the secretory system.
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PMID:Insulin secretory responses of a clonal cell line of simian virus 40-transformed B cells. 302 78

Effects of constant and pulsatile i.v. insulin delivery were examined in seven healthy subjects by means of euglycemic clamp technique. Each subject received constant insulin infusion (0.175 mU/kg.min) or insulin pulses at 12-min intervals (2.1 mU/kg) in randomized order for 8-h periods (08.00-16.00 h). Endogenous secretion of insulin was inhibited by concomitant administration of somatostatin (300 micrograms/h). Serum insulin concentrations during constant infusion (12 +/- 1 microU/ml) did not differ from basal values (11 +/- 1 microU/ml). Pulsatile insulin delivery resulted in oscillations of mean concentrations between values of about 10 and 20 microU/ml. Mean blood glucose concentrations during experiments were kept at 80 +/- 1 mg/dl, irrespective of the mode of insulin administration. Moreover, dextrose requirements for maintenance of these glucose concentrations did not differ over the hole periods of examination. We conclude that effects of constant and pulsatile delivery of basal amounts of insulin are not different. This at least applies to peripheral, short-term insulin administration in somatostatin-treated normal man, during an euglycemic clamp.
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PMID:Similar effects of pulsatile and constant intravenous insulin delivery. 328 66

The possibility that somatostatin has a direct inhibitory effect on intestinal D-glucose absorption was studied in rats using intact intestinal loops and everted jejunal segments. Somatostatin infusion in vivo produced a significant fall in plasma glucose concentration (P less than 0.001) and a fall in pooled plasma insulin concentration to 51% of control values. However, somatostatin infusion did not alter significantly from control values the rate of glucose disappearance from the perfused jejunal lumen in vivo or the appearance of gut-derived plasma glucose. The lack of an inhibitory effect of somatostatin on glucose absorption in vivo was confirmed using two in vitro studies. When increasing concentrations of somatostatin (0-10(4) ng/ml-1) were added to both mucosal and serosal solutions, no significant differences were seen for net transmural flux or unidirectional flux of D-glucose in everted jejunal segments. These studies suggest that somatostatin in the rat does not influence plasma glucose concentration by inhibiting intestinal glucose transport at physiological concentrations of glucose and over a wide range of somatostatin concentrations.
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PMID:The effect of somatostatin on the intestinal transport of glucose in vivo and in vitro in the rat. 610 12

Specific radioimmunoassay were used to measure somatostatin and vasoactive peptide in portal and peripheral plasma from conscious dogs prepared with indwelling portal catheters. In six animals with intact stomachs, a test meal induced a significant rise of portal and peripheral somatostatin, while the significant response of vasoactive intestinal peptide in portal plasma was not reflected in peripheral blood. Similar somatostatin and vasoactive intestinal peptide responses were observed in six dogs previously submitted to antrectomy and Billroth I anastomosis, when given the same test meal, while the gastrin response was 20% of the response in the intact dogs (P < 0.01). The effects of intragastric instillation of 300 ml dextrose, casein hydrolysate, and Intralipid, adjusted to 300 mosmol/kg and pH 7.0, were studied in six dogs with intact stomachs. Casein and Intralipid induced significant increases of somatostatin in portal and peripheral plasma, while VIP increased after Intralipid only, both in portal and peripheral blood. Dextrose resulted in no significant variation of either peptide in portal or in systemic plasma. Intraduodenal infusion of isotonic bile induced a significant release of somatostatin, both in portal and peripheral plasma, but no significant vasoactive intestinal peptide response. These results indicate that several factors can evoke a significant release of somatostatin in dogs, and that the variations of the peptide concentration in portal plasma are reflected in peripheral blood. Among the factors tested, only intragastric fat evoked a vasoactive intestinal peptide response that could be measured in peripheral blood.
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PMID:Effects of test meal, intragastric nutrients, and intraduodenal bile on plasma concentrations of immunoreactive somatostatin and vasoactive intestinal peptide in dogs. 610 20

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 2-deoxy-D-glucose (2-DG) on plasma levels of somatostatin-like immunoreactivity (SLI) were examined in conscious normal dogs. After an iv infusion of 2-DG (400 mg/kg . h for 15 min), plasma SLI rose significantly from a mean baseline of 130 +/- 5 pg/ml (mean +/- SEM) to a mean peak of 204 +/- 25 pg/ml (P less than 0.005) at 25 min. Plasma insulin and glucagon also increased significantly. Atropine (200 microgram/kg . h for 35 min, iv) and hexamethonium (5 mg/kg, iv) markedly suppressed the SLI response to 2-DG, suggesting that it might be mediated, at least in part, by the autonomic nervous system. In contrast, the plasma insulin and plasma glucagon responses to this glucose analog were only slightly affected by atropine or hexamethonium pretreatment. Carbachol (0.2 mg, sc) caused a mean maximal increase in SLI of 43 +/- 14% (P less than 0.005) and atropine (200 micrograms/kg . h, iv) caused a mean maximal decrease of 25 +/- 2% (P less than 0.001) from the respective baseline levels. Plasma insulin and glucagon rose promptly after carbachol and were unchanged by atropine. To assess th contribution of 2-DG-stimulated gastric acid secretion in the 2-DG-induced SLI rise 2-DG was infused during the infusion of the H2-receptor antagonist cimetidine (3.0 mg/kg . h). Plasma SLI, nevertheless, increased significantly from a mean baseline of 112 +/- 6 pg/ml to a mean peak of 158 +/- 19 pg/ml (P less than 0.005) at 20 min, although the magnitude of the response was substantially reduced (P = NS). These observations suggest that in the conscious dog, 2-DG stimulates SLI secretion in part via cholinergic mechanism.
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PMID:Effect of 2-deoxy-D-glucose on plasma somatostatin levels in conscious dogs. 611 May 37

To investigate how the D-cell recognizes the glucose stimulus, the hormone response to (1) glucose, (2) the trioses glyceraldehyde and dihydroxyacetone, (3) the metabolic blocker, mannoheptulose, and (4) the low- or nonmetabolized sugars galactose, fructose, or ribose were studied using the isolated dog pancreas. We found (1) a sigmoidal relationship between extracellular glucose concentrations and the somatostatin release. The threshold concentration was around 5 mM and the largest increase in somatostatin release occurs between 5 and 10 mM of glucose. (2) Glyceraldehyde at concentrations ranging between 1.25 and 5 mM stimulated the release of somatostatin, whereas the higher concentrations of 10 and 20 mM were suppressive. Dihydroxyacetone (11 mM), also initiated somatostatin release in the absence of glucose. Both of the trioses stimulated B- and inhibited A-cell secretion. (3) Mannoheptulose (5 mM) attenuated somatostatin and insulin secretion to 8.3 mM glucose, while it augmented glucagon output. In contrast, mannoheptulose (5 mM) did not affect D-, A-, or B-cell responses to glyceraldehyde (5 mM) in the absence of glucose. (4) The somatostatin, insulin, and glucagon release remained unchanged when 8.3 mM of either galactose, fructose, or ribose was added. The results suggest that the initiation of glucose-mediated D- as well as A- and B-cell responses depends on the metabolism of the sugar.
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PMID:Pancreatic D-cell recognition of D-glucose: studies with D-glucose, D-glyceraldehyde, dihydroxyacetone, D-mannoheptulose, D-fructose, D-galactose, and D-ribose. 611 Jun

3-O-(2-Acetamido-3,4,6-tri-O-acetyl-2-deoxy-beta-D-glucopyranosyl)-N- (tert-butyloxycarbonyl)-L-serine was synthesized and condensed by the solid-phase procedure to give the sequence Gly-[beta-D-GlcpNAc-(1 leads to 3)-Ser]-Ala-OH and beta-D-GlcpNAc-(1 leads to 3)-Ser-13-somatostatin. The synthetic glycopeptides appeared homogeneous on t.l.c. and l.c. examination and showed the correct amino acid composition and 2-amino-2-deoxy-D-glucose content. The structure of Gly-[beta-D-GlcpNAc-(1 leads to 3)-Ser]-Ala-OH was further confirmed by mass spectrometry of the N-acetyl permethyl derivative, and by n.m.r. spectroscopy.
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PMID:Synthesis of a glycotripeptide and a glycosomatostatin containing the 3-O-(2-acetamido-2-deoxy-beta-D-glucopyranosyl)-L-serine residue. 611 52


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