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Indomethacin and salicylate decrease epinephrine-induced glycogenolysis.

J D Miller, S Ganguli, R Artal

    Metabolism: Clinical and Experimental
    |February 1, 1985
    PubMed
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    Inhibitors of arachidonic acid metabolism, indomethacin and salicylate, reduced the immediate rise in hepatic glucose production stimulated by epinephrine in dogs. This suggests a role for arachidonic acid metabolites in early glucose regulation during stress responses.

    Area of Science:

    • Endocrinology
    • Metabolic Research
    • Pharmacology

    Background:

    • Epinephrine (E) acutely increases hepatic glucose production (Ra) via glycogenolysis, followed by gluconeogenesis.
    • The role of arachidonic acid metabolites in mediating E-stimulated Ra remains unclear.

    Purpose of the Study:

    • To investigate the involvement of arachidonic acid metabolites in the immediate hepatic glucose production during epinephrine stimulation.
    • To determine if inhibiting arachidonic acid metabolism affects E-induced glucose release in vivo.

    Main Methods:

    • Epinephrine was infused in trained conscious dogs before and during administration of indomethacin (INDO) and salicylate (S).
    • Hepatic glucose production (Ra) and glucose utilization (Rd) were measured using isotope dilution with 3-3H-glucose.

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  • Plasma glucose levels were monitored to assess changes in glucose homeostasis.

    • Main Results:

    • Epinephrine infusion significantly increased plasma glucose and Ra in control dogs.
    • Indomethacin and salicylate treatments attenuated the initial rise in plasma glucose and Ra at 10-20 minutes post-epinephrine infusion.
    • No significant differences in Ra, Rd, or insulin levels were observed after 20 minutes of epinephrine infusion between groups.

    Conclusions:

    • Arachidonic acid metabolites appear to play a role in the early phase of epinephrine-stimulated hepatic glucose production.
    • Inhibition of arachidonic acid metabolism blunts the acute glycemic response to epinephrine.
    • These findings highlight a potential mechanism linking inflammatory pathways to glucose metabolism regulation.