PMID: 7012876Mar 1, 1981Paper

Prostaglandins and the alpha-cell

Prostaglandins and Medicine
D GiuglianoF D'Onofrio

Abstract

Experimental evidence has recently accumulated indicating that administration of some prostaglandins (PGs), particularly those of the E series, can evoke release of glucagon by the pancreatic alpha-cells. Virtually, all the in vitro studies (isolated perfused rat pancreas, isolated guinea-pig islets) agree that PGs can increase both basal and stimulated glucagon release. On the other hand, inhibition of PG synthesis with indomethacin blocks glucagon release. In rats and in normal humans, PGE1, but not PGA2 or PGF2a, causes a progressive rise of plasma glucagon levels. While in the rat this response seems independent of the adrenergic nervous system, in man the hyperglucagonemia induced by PGE1 is easily suppressed by propranolol, suggesting an interaction between the prostaglandin and the beta-receptors of the alpha-cell. Studies with inhibitors of PG synthesis in vivo have yielded conflicting results, depending on the particular experimental protocol used and on the type of inhibitor tested. In normal humans, it seems that acetylsalicylic acid (ASA) has no effect on glucagon response to arginine, tolbutamide and insulin-induced hypoglycemia. Conversely, a stimulator of PG synthesis, such as furosemide, increases glucagon respo...Continue Reading

References

Sep 1, 1977·The Journal of Clinical Investigation·R P Robertson, M Chen
Feb 1, 1977·Metabolism: Clinical and Experimental·F CavagniniP Vigo
Feb 1, 1976·Metabolism: Clinical and Experimental·L Saccà, G Perez
Nov 1, 1972·Biochemical and Biophysical Research Communications·M Hamberg
Sep 1, 1973·The Journal of Clinical Endocrinology and Metabolism·J E GerichP H Forsham
Mar 1, 1980·The Journal of Clinical Investigation·R A RizzaJ E Gerich

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Citations

Mar 1, 1983·Prostaglandins·Y C Kim, R G Brodows
Aug 29, 2016·Cardiovascular Diabetology·Antonio CerielloEdoardo Gronda
Apr 1, 1985·Klinische Wochenschrift·M GoerigG Schettler

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