Desensitization of β-adrenergic receptors in adipocytes causes increased insulin sensitivity of glucose transport

Allan Green, Richard M. Carroll, Susan B. Dobias

    Research output: Contribution to journalArticlepeer-review

    21 Scopus citations


    To determine the effect of desensitization of adipocyte β-adrenergic receptors on insulin sensitivity, rats were continuously infused with isoproterenol (50 or 100 μg · kg-1 · h-1) for 3 days by osmotic minipumps. Epididymal adipocytes were isolated. The cells from treated animals were desensitized to isoproterenol, as determined by response of lipolysis (glycerol release). Binding of [125I]iodocyanopindolol was decreased by ~80% in adipocyte plasma membranes isolated from treated rats, indicating that β-adrenergic receptors were downregulated. Cellular concentrations of G(s)α and G(i)α were not altered. Insulin sensitivity was determined by measuring the effect of insulin on glucose transport (2- deoxy[3H]glucose uptake). Cells from the isoproterenol-infused rats were markedly more sensitive to insulin than those from control rats. This was evidenced by an ~50% increase in maximal glucose transport rate in cells from the high-dose isoproterenol-treated rats and by an ~40% decrease in the half-maximal effective concentration of insulin in both groups. 125I- labeled insulin binding to adipocytes was not altered by the isoproterenol infusions, indicating that desensitization of β-adrenergic receptors results in tighter coupling between insulin receptors and stimulation of glucose transport.

    Original languageEnglish (US)
    Pages (from-to)E271-E276
    JournalAmerican Journal of Physiology - Endocrinology and Metabolism
    Issue number2 34-2
    StatePublished - Aug 1996


    • catecholamines
    • insulin

    ASJC Scopus subject areas

    • Endocrinology, Diabetes and Metabolism
    • Physiology
    • Physiology (medical)


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