Cyclic AMP-dependent stimulation of somatostatin secretion by isolated rat islets of Langerhans

Barden, Nicholas; Alvarado-Urbina, Gabriel; Côté, Jean-Pierre; Dupont, André

doi:10.1016/0006-291x(76)90907-4

Cited by 46 publications

(15 citation statements)

References 9 publications

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“…Therefore, if controls occur at the somatostatin mRNA and protein synthesis level, then what factors are responsible? Earlier studies suggested that glucose could be involved; indeed, high glucose stimulated somatostatin release from monolayer cultures of neonatal rat pancreas (17) and from rat isolated islets (42), observations not confirmed in another study (43). Increased somatostatin secretion could trigger somatostatin synthesis, and glucose was shown (44) to regulate pancreatic preprosomatostatin I expression as it increased somatostatin release from rainbow trout Brockmann bodies.…”

Section: Discussionmentioning

confidence: 96%

Regulation of Rat Pancreatic CCKB Receptor and Somatostatin Expression by Insulin

Julien

Lainé²,

Morisset³

2004

Diabetes

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The cholecystokinin B receptor (CCK B R) is localized on pancreatic endocrine somatostatin ␦-cells. Pancreatic somatostatin content was increased in diabetic rats. The mechanisms involved in this phenomenon are unknown, and we believe insulin is involved. In this study, four groups of rats were used: controls, streptozotocininduced diabetic, streptozotocin-induced diabetic with insulin, and streptozotocin-induced diabetic with insulin and its cessation. Rats were killed after 7-28 days of treatment for diabetes, and somatostatin mRNA expression and pancreatic somatostatin content, CCK B R mRNA and protein expression evaluation in total pancreas and purified islets, and the cellular localization of somatostatin and CCK B R in islets was measured. Data indicate that diabetes is established after 7 days, is controlled by insulin, and reappears after treatment cessation. Pancreatic somatostatin mRNA expression and somatostatin content were increased during diabetes, normalized during insulin treatment, and reaugmented after treatment cessation. Gland and islet CCK B R mRNA and protein almost disappeared during diabetes; CCK B mRNA reappeared in response to insulin, but the protein did not. Confocal microscopy confirmed data obtained on somatostatin and CCK B R as established biochemically in the course of the treatments. In conclusion, these data strongly suggest that insulin can negatively control pancreatic somatostatin mRNA and hormone content and positively control CCK B R mRNA; the CCK B R protein appears to be delayed. Diabetes 53: 1526 -1534, 2004 D uring the 1970s, major changes were observed in the metabolism of pancreatic somatostatin during diabetes development in human and experimental animals; these modifications included increased secretion, tissue contents, and ␦-cell population (1-12). On the contrary, it was also reported (13,14) that in diabetic mice mutants (ob/ob and db/db), pancreatic somatostatin content was decreased, along with a reduction in somatostatin cells within the islet. It was later suggested that in streptozotocin (STZ)-induced diabetic rats, regulation of somatostatin gene transcription was targeted to the pancreas and stomach but not to the other somatostatin-producing tissues (15).The role played by insulin in somatostatin release remains controversial. Indeed, insulin can stimulate somatostatin release from perfused chicken pancreas-duodenum (16); however, data from monolayer cultures of neonatal rat pancreas (17) and isolated dog pancreas (18) clearly show that insulin fails to induce somatostatin release. In anesthetized normal and diabetic dogs, insulin infusion or injection was associated with an immediate reduction of the venous pancreaticoduodenal release of somatostatin (19). All of these differences could be explained by the different models used to study somatostatin release.Cholecystokinin (CCK), a duodenal hormone released into the bloodstream after meal ingestion, is recognized as the major hormonal factor involved in the regulation of pancreatic exocrine secretio...

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Section: Discussionmentioning

confidence: 96%

Regulation of Rat Pancreatic CCKB Receptor and Somatostatin Expression by Insulin

Julien

Lainé²,

Morisset³

2004

Diabetes

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“…Glycerol failed to stimulate SLI secretion. Glucose lowers peripheral SLI levels in normal dogs despite increased pancreatic SLI release (13,27), although it has been reported to stimulate somatostatin in some (28)(29)(30) but not other (31,32) in vitro studies. Amino acid mixture stimulates SLI release from the canine pancreas (29) but not from the stomach and peripheral venous levels of SLI do not rise after intravenous infusion of a 15-amino acid mixture in conscious normal dogs (unpublished observation).…”

Section: Discussionmentioning

confidence: 99%

Evidence for a Role of Free Fatty Acids in the Regulation of Somatostatin Secretion in Normal and Alloxan Diabetic Dogs

Wasada¹,

Howard²,

Dobbs³

et al. 1980

J. Clin. Invest.

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A B S T R A C T To investigate the effect ofacute elevation ofplasma free fatty acids (FFA) on the secretion of splanchnic somatostatin-like immunoreactivity (SLI), the peripheral venous, pancreatic, and gastric venous effluent levels of SLI were measured in normal and chronic alloxan diabetic dogs before and after the infusion of a fat emulsion supplemented with heparin. In normal conscious dogs heparin injected during the infusion of a fat emulsion elevated FFA levels from a mean (+SE) base-line level of 0.7+0.1 meq/liter to a peak value of 1.5±0.1 meq/liter (P < 0.001) and plasma SLI rose from a mean (±SE) base-line value of 145±7 pg/ml to a peak of 253±44 pg/ml (P < 0.05). Neither the infusion of glycerol, of fat emulsion without heparin, of heparin alone nor of saline itself had an effect on either the plasma level of FFA or SLI. In another group of anesthetized dogs with surgically implanted catheters the administration of fat emulsion plus heparin was accompanied by more than a twofold rise in the concentration of SLI in the venous effluent of the pancreas and of the gastric fundus and antrum in association with an elevation of FFA levels. In a group of conscious diabetic dogs fat emulsion plus heparin raised FFA from a mean base-line level of 1.2±0.2 to 1.6±0.3 meq/liter (P < 0.05) and SLI rose from a mean base-line level of 185±9 pg/ml to a peak value of 310±44 pg/ml (P < 0.01). Although SLI levels were significantly greater than in normal dogs at several time points after the rise in FFA, the magnitude of the increment in diabetic dogs did not differ from normal. These results demonstrate that a rise in FFA levels is a potent stimulus for SLI secretion from the pancreas Dr. Unger is a Senior Medical Investigator, Veterans

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“…If so, the A-, B-, and D-cells of the islets of Langerhans would have an influence over all routes through eas (9), and which fuels move into and out of the extracellular rden et al space. In particular, coordinated responses of panlucose (20). creatic somatostatin and insulin secretion would For the first permit coordination of the rates at which exogenous to 20 mM nutrients enter and leave the extracellular space iM leucine, and thereby enable the islets to regulate their turnill of which over and concentrations (11).…”

Section: Effectmentioning

confidence: 99%

Release of immunoreactive somatostatin from the pancreas in response to glucose, amino acids, pancreozymin-cholecystokinin, and tolbutamide.

Ipp¹,

Dobbs²,

Arimura³

et al. 1977

J. Clin. Invest.

168

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A B S T R A C T 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 doseresponse 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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Cyclic AMP-dependent stimulation of somatostatin secretion by isolated rat islets of Langerhans

Cited by 46 publications

References 9 publications

Regulation of Rat Pancreatic CCKB Receptor and Somatostatin Expression by Insulin

Regulation of Rat Pancreatic CCKB Receptor and Somatostatin Expression by Insulin

Evidence for a Role of Free Fatty Acids in the Regulation of Somatostatin Secretion in Normal and Alloxan Diabetic Dogs

Release of immunoreactive somatostatin from the pancreas in response to glucose, amino acids, pancreozymin-cholecystokinin, and tolbutamide.

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