Calcium mobilization, prostaglandin E2 and α2-adrenoceptor modulation of glucose utilization and insulin secretion in pancreatic islets

Laychock, Suzanne G.; Bilgin, Suna

doi:10.1016/0006-2952(89)90096-8

Cited by 10 publications

(3 citation statements)

References 38 publications

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“…This is because the inhibitory effects of RX871024 are not seen in the isolated perfused rat pancreas ( Zaitsev et al ., 1996 ; Efanova et al ., 1998b ) nor in freshly isolated, perifused, islets (Chan & Morgan; unpublished observations) where paracrine influences are minimized by the flow of perfusate. One important paracrine inhibitor of insulin secretion is prostaglandin E 2 (PGE 2 ; Robertson, 1986 ; 1988 ; Laychock & Bilgin, 1989 ; Metz, 1998; 1991 ; Metz et al ., 1991 ; Morgan & Montague, 1992 ) and it has been reported that the levels of this agent are markedly reduced in islets during conditions of fasting ( Tadayyon et al ., 1990 ). Thus, we investigated the ability of RX871024 to regulate insulin secretion from islets of animals deprived of food for increasing periods of time.…”

Section: Resultsmentioning

confidence: 99%

Multiple effector pathways regulate the insulin secretory response to the imidazoline RX871024 in isolated rat pancreatic islets

Mourtada

Chan

Smith

et al. 1999

British J Pharmacology

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1 When isolated rat islets were cultured for 18 h prior to use, the putative imidazoline binding site ligand, RX871024 caused a dose-dependent increase in insulin secretion at both 6 mM and 20 mM glucose. By contrast, a second ligand, efaroxan, was ineective at 20 mM glucose whereas it did stimulate insulin secretion in response to 6 mM glucose. 2 Exposure of islets to RX871024 (50 mM) for 18 h, resulted in loss of responsiveness to this reagent upon subsequent re-exposure. However, islets that were unresponsive to RX871024 still responded normally to efaroxan. 3 The imidazoline antagonist, KU14R, blocked the insulin secretory response to efaroxan, but failed to prevent the stimulatory response to RX871024. 4 By contrast with its eects in cultured islets, RX871024 inhibited glucose-induced insulin release from freshly isolated islets. Efaroxan did not inhibit insulin secretion under any conditions studied. 5 In freshly isolated islets, the eects of RX871024 on insulin secretion could be converted from inhibitory to stimulatory, by starvation of the animals. 6 Inhibition of insulin secretion by RX871024 in freshly isolated islets was prevented by the cyclooxygenase inhibitors indomethacin or¯urbiprofen. Consistent with this, RX871024 caused a marked increase in islet PGE 2 formation. Efaroxan did not alter islet PGE 2 levels. 7 The results suggest that RX871024 exerts multiple eects in the pancreatic b-cell and that its eects on insulin secretion cannot be ascribed only to interaction with a putative imidazoline binding site.

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Section: Resultsmentioning

confidence: 99%

Multiple effector pathways regulate the insulin secretory response to the imidazoline RX871024 in isolated rat pancreatic islets

Mourtada

Chan

Smith

et al. 1999

British J Pharmacology

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“…Insulin release from pancreatic islets is antagonized by endogenous PG production and by exogenous PGE2 (Robertson, 1974(Robertson, , 1983Turk et al, 1988;Laychock & Bilgin, 1989). The negative influence of PGE2 on insulin release appears to be modulated in part by the receptor-mediated inhibition of adenylate cyclase (Robertson et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

“…An inhibitory G-protein mediates the inhibitory effects of PGE on insulin release, since pertussis toxin reverses the inhibitory response in islets and insulinoma cells (Robertson et al, 1987). However, PGE2 also inhibits glucose oxidation, and a pertussis-toxin-inhibitable process modulates the glucose-oxidation response (Laychock, 1989;Laychock & Bilgin, 1989). Since glucose utilization in islets is not modulated by cyclic AMP (Laychock, 1987), PGE2 may have an effect on a transduction mechanism(s) other than adenylate cyclase which modulates metabolism and insulin release.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 inhibits phosphoinositide metabolism in isolated pancreatic islets

Laychock

1989

Biochemical Journal

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Isolated islets of the rat labelled with myo-[3H]inositol showed decreased accumulation of total inositol phosphates (InsPs) and [3H]polyphosphoinositide hydrolysis in response to glucose after preincubation with prostaglandin E2 (PGE2). The response was concentration-dependent and specific for PGE2. PGE2 did not affect basal [3H]phosphoinositide hydrolysis or InsPs accumulation. Pertussis-toxin pretreatment antagonized the response to PGE2, whereas 8-bromo cyclic AMP was without effect. The PGE2-induced decrease in InsPs may contribute to the suppression of insulin secretion.

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Electrophysiology of the β Cell and Mechanisms of Inhibition of Insulin Release

Dunne

Ämmälä

Straub

et al. 2001

Comprehensive Physiology

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The sections in this article are: Ion Channels in Insulin‐Secreting Cells Adenosine Triphosphate–Sensitive Potassium Channels Extracellular Control of Adenosine Triphosphate‐Sensitive Potassium Channel Function Therapeutic Manipulation by Modulators of Adenosine Triphosphate‐Sensitive Potassium Channels Architecture of the β‐cell Adenosine Triphosphate‐Sensitive Potassium Channel Calcium‐Selective Ion Channels Voltage‐Gated Sodium Channels Voltage‐Gated Potassium Channels Voltage‐Independent Potassium Channels Nonselective Cation Channels Anion‐Selective Channels Ionic Defects of β‐Cell Function Persistent Hyperinsulinemic Hypoglycemia of Infancy Altered Ionic Control of β Cells and Hypersecretion of Insulin Correlation of Gene Defects in the Adenosine Triphosphate‐Sensitive Potassium Channel with Persistent Hyperinsulinemic Hypoglycemia of Infancy Clinical Therapy for Persistent Hyperinsulinemic Hypoglycemia of Infancy Implications for Diabetes Mellitus Stimulus‐Secretion Coupling Mechanisms Other Than Depolarization Novel Methods for the Measurement of Insulin Secretion Capacitance Amperometry and Voltametry Calcium and Exocytosis Cyclic Adenosine Monophosphate and Exocytosis Effects of Phospholipases and Protein Kinases C and A Sulfonylureas and Exocytosis G Proteins and Exocytosis Other Modulators of Exocytosis Modeling Calcium‐, Cyclic, and Adenosine Monophosphate–, and Guanosine Triphosphate–Dependent Exocytosis Molecular Mechanisms of Exocytosis in the β Cell Receptor‐Mediated Inhibition of Insulin Release: Early and Late Effects Involvement of G Proteins Receptor–G Protein Interactions Inhibitory Mechanisms Adenosine Triphosphate–Sensitive Potassium Channel Activation and Membrane Repolarization Calcium Channel Inhibition Inhibition of Adenylate Cyclase Inhibition at a Distal Site G Protein–Target Interactions Adenosine Triphosphate–Sensitive Potassium Channel L‐Type Calcium Channels Adenylate Cyclase Distal Inhibitory Site Other Possible Mechanisms Inhibition of Glucose Metabolism Inhibition of Fatty Acid Metabolism Stimulation of Calcium–Adenosine Triphosphatase Activity Cyclic Guanosine Monophosphate Cytoskeleton Summary of Inhibitory Mechanisms

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Calcium mobilization, prostaglandin E2 and α2-adrenoceptor modulation of glucose utilization and insulin secretion in pancreatic islets

Cited by 10 publications

References 38 publications

Multiple effector pathways regulate the insulin secretory response to the imidazoline RX871024 in isolated rat pancreatic islets

Multiple effector pathways regulate the insulin secretory response to the imidazoline RX871024 in isolated rat pancreatic islets

Prostaglandin E2 inhibits phosphoinositide metabolism in isolated pancreatic islets

Electrophysiology of the β Cell and Mechanisms of Inhibition of Insulin Release

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