Effects of Prostaglandin Ei and of Epinephrine on the Dynamics of Insulin Release<i>in Vitro</i><sup>1</sup>

Burr, Ian M.; Sharp, Robert A.

doi:10.1210/endo-94-3-835

Cited by 42 publications

(12 citation statements)

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“…We have reported previously that treatment of pancreatic ␤ cells with exogenous PGE 2 causes a decrease in insulin secretion in vitro (1)(2)(3)(4)(5)(6) and in vivo (7)(8)(9)(10)(11) and that inhibitors of endogenous prostaglandin synthesis augment glucose-induced insulin secretion in vitro (3,26) and in vivo (9 -11). The single exception to the latter generalization has been indomethacin.…”

Section: Discussionmentioning

confidence: 99%

“…1 is known to be an inhibitor of glucose-induced insulin secretion from studies in a ␤ cell line (1,2) and isolated and neonatal islets of Langerhans (3)(4)(5)(6) as well as in vivo in both animal (7,8) and human (9 -11) studies. These findings have been reinforced by studies in which inhibitors of cyclooxygenase, hence PGE 2 synthesis, have augmented glucose-induced insulin secretion.…”

Section: Prostaglandin E 2 (Pge 2 )mentioning

confidence: 99%

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Prostaglandin E2 Mediates Inhibition of Insulin Secretion by Interleukin-1β

Tran

Gleason

Poitout

et al. 1999

Journal of Biological Chemistry

107

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Interleukin-1␤ (IL-1␤) and prostaglandin E 2 (PGE 2 ), frequently co-participants in inflammatory states, are two well recognized inhibitors of glucose-induced insulin secretion. Previous reports have concluded that the inhibitory effects of these two autacoids on pancreatic ␤ cell function are not related because indomethacin, a potent prostaglandin synthesis inhibitor, does not prevent IL-1␤ effects. However, indomethacin is not a specific cyclooxygenase inhibitor, and its other pharmacologic effects are likely to inhibit insulin secretion independently. Since we recently observed that IL-1␤ induces cyclooxygenase-2 (COX-2) gene expression and PGE 2 synthesis in islet ␤ cells, we have reassessed the possibility that PGE 2 mediates IL-1␤ effects on ␤ function. By using two cell lines (HIT-T15 and ␤HC13) as well as Wistar rat isolated pancreatic islets, we examined the ability of two COX-2-specific antagonists, NS-398 and SC-236, to prevent IL-1␤ inhibition of insulin secretion. Both drugs prevented IL-1␤ from inducing PGE 2 synthesis and inhibiting insulin secretion; adding back exogenous PGE 2 re-established inhibition of insulin secretion in the presence of IL-1␤. We also found that EP3, the PGE 2 receptor subtype whose post-receptor effect is to decrease adenylyl cyclase activity and, thereby, insulin secretion, is the dominant mRNA subtype expressed. We conclude that endogenous PGE 2 mediates the inhibitory effects of exogenous IL-1␤ on ␤ cell function. Prostaglandin E 2 (PGE 2 )1 is known to be an inhibitor of glucose-induced insulin secretion from studies in a ␤ cell line (1, 2) and isolated and neonatal islets of Langerhans (3-6) as well as in vivo in both animal (7,8) and human (9 -11) studies. These findings have been reinforced by studies in which inhibitors of cyclooxygenase, hence PGE 2 synthesis, have augmented glucose-induced insulin secretion. The only discordant result in the latter category of studies has been observed when indomethacin was used as the cyclooxygenase inhibitor. This discrepant result can be attributed to other effects of indomethacin that would be expected to inhibit insulin secretion through adverse effects on exocytosis that are unrelated to its effects on prostaglandin synthesis (12).Interleukin-1␤ (IL-1␤) has been reported to have major inhibitory effects on ␤ cell function, especially under conditions of high glucose concentrations and prolonged exposure to this cytokine (13)(14)(15)(16). This is an especially relevant observation because many reports suggest that IL-1␤ is an important force in the pathogenesis of diabetes mellitus (17,18). Previously, studies have concluded that endogenous PGE 2 does not play a participatory role in the adverse effects of IL-1␤ on ␤ cell function (5, 6). Ironically, however, the drug that was chosen to test this hypothesis and found not to reverse IL-1␤ inhibitory effects on insulin secretion was indomethacin, which itself has independent inhibitory actions on ␤ cell exocytosis (12).Recently, it has been appreciated that the pancreatic is...

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Section: Discussionmentioning

confidence: 99%

Section: Prostaglandin E 2 (Pge 2 )mentioning

confidence: 99%

Prostaglandin E2 Mediates Inhibition of Insulin Secretion by Interleukin-1β

Tran

Gleason

Poitout

et al. 1999

Journal of Biological Chemistry

107

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“…Stimulatory as well as inhibitory effects of various prostaglandins on the secretion of insulin and glucagon have been described in vitro (8)(9)(10) and in vivo. Whereas iv administration of prostaglandins Ei, E 2 , F 2 «, and Ai does not change basal insulin secretion (11,12), iv infusion of PGE 2 inhibits glucose-induced, but not arginine-induced, insulin release (13).…”

Section: Discussionmentioning

confidence: 99%

Unchanged Arginine-Induced Stimulation of Insulin, Glucagon, Growth Hormone, and Prolactin after Pretreatment with Indomethacin in Normal Man*

Vierhapper

Bratusch-Marrain

Waldhäusl

1980

The Journal of Clinical Endocrinology & Metabolism

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The arginine-induced release of insulin, glucagon, GH, and PRL was studied in eight normal male volunteers. Pretreatment with indomethacin (150 mg for 3 days) failed to modify the effect of arginine on the release of these hormones. As both indomethacin and acetylsalicylic acid are potent inhibitors of the endogenous prostaglandin synthesis, these results indicate that the effect of acetylsalicylic acid on insulin and glucagon secretion, as described by others, seems to be unrelated to the suppression of endogenous prostaglandin synthesis.

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“…In vitro experiments in rat islets showed an opposite inhibitory effect of PGE 1 on insulin release under high glucose environment (300 mg/dl). 62 …”

Section: A N U S C R I P Tmentioning

confidence: 99%

Prophylactic L-arginine and ibuprofen delay the development of tactile allodynia and suppress spinal miR-155 in a rat model of diabetic neuropathy

El-Lithy

El-Bakly

Matboli

et al. 2016

Translational Research

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Effects of Prostaglandin Ei and of Epinephrine on the Dynamics of Insulin Releasein Vitro¹

Cited by 42 publications

References 0 publications

Prostaglandin E2 Mediates Inhibition of Insulin Secretion by Interleukin-1β

Prostaglandin E2 Mediates Inhibition of Insulin Secretion by Interleukin-1β

Unchanged Arginine-Induced Stimulation of Insulin, Glucagon, Growth Hormone, and Prolactin after Pretreatment with Indomethacin in Normal Man*

Prophylactic L-arginine and ibuprofen delay the development of tactile allodynia and suppress spinal miR-155 in a rat model of diabetic neuropathy

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Effects of Prostaglandin Ei and of Epinephrine on the Dynamics of Insulin Releasein Vitro1

Cited by 42 publications

References 0 publications

Prostaglandin E2 Mediates Inhibition of Insulin Secretion by Interleukin-1β

Prostaglandin E2 Mediates Inhibition of Insulin Secretion by Interleukin-1β

Unchanged Arginine-Induced Stimulation of Insulin, Glucagon, Growth Hormone, and Prolactin after Pretreatment with Indomethacin in Normal Man*

Prophylactic L-arginine and ibuprofen delay the development of tactile allodynia and suppress spinal miR-155 in a rat model of diabetic neuropathy

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Product

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Effects of Prostaglandin Ei and of Epinephrine on the Dynamics of Insulin Releasein Vitro¹