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Prostaglandins and the alpha-cell

D Giugliano, R Torella, F D'Onofrio

    Prostaglandins and Medicine
    |March 1, 1981
    PubMed
    Summary
    This summary is machine-generated.

    Prostaglandins (PGs), especially PGE1, stimulate glucagon release from pancreatic alpha-cells. This effect in humans involves beta-receptors, suggesting PGs play a role in regulating glucagon secretion.

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    Area of Science:

    • Endocrinology
    • Cell Biology
    • Pharmacology

    Background:

    • Emerging evidence suggests prostaglandins (PGs) influence glucagon secretion.
    • Pancreatic alpha-cells are implicated as a site of PG action.

    Purpose of the Study:

    • To investigate the role of prostaglandins (PGs) in regulating glucagon release.
    • To explore the interaction between PGs and alpha-cell function.

    Main Methods:

    • In vitro studies using isolated perfused rat pancreas and guinea-pig islets.
    • In vivo studies in rats and humans involving administration of various prostaglandins (PGE1, PGA2, PGF2a) and inhibitors of PG synthesis (indomethacin, acetylsalicylic acid).
    • Assessment of plasma glucagon levels and glucagon responses to various stimuli (arginine, tolbutamide, insulin-induced hypoglycemia, salbutamol).

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    Main Results:

    • In vitro studies consistently show PGs increase basal and stimulated glucagon release; indomethacin inhibits this release.
    • PGE1, but not PGA2 or PGF2a, increases plasma glucagon in rats and humans.
    • In humans, PGE1-induced hyperglucagonemia is suppressed by propranolol, indicating beta-receptor involvement.

    Conclusions:

    • Prostaglandins, particularly those of the E series, play a significant role in controlling glucagon release.
    • Evidence supports an interaction between prostaglandins and beta-adrenergic receptors on pancreatic alpha-cells.
    • Further research is needed to clarify the in vivo effects of PG synthesis inhibitors due to conflicting results.