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Related Experiment Videos

Glucocorticoids regulate insulin binding in a rat glial cell line.

F Montiel, J Ortiz-Caro, A Villa

    Endocrinology
    |July 1, 1987
    PubMed
    Summary

    Glucocorticoids, like dexamethasone, reduce insulin receptor levels in C6 rat glioma cells. Protein synthesis is required for this effect, suggesting glucocorticoids deplete both membrane and total cellular receptors.

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    Area of Science:

    • Endocrinology
    • Cell Biology
    • Neuroscience

    Background:

    • Insulin receptors are crucial for cellular signaling.
    • Glucocorticoids are known to influence various cellular processes.
    • Regulation of insulin receptor by glucocorticoids in glioma cells is not fully understood.

    Purpose of the Study:

    • To investigate the effect of glucocorticoids on insulin receptor regulation in C6 rat glioma cells.
    • To determine the mechanism by which glucocorticoids modulate insulin receptor expression.

    Main Methods:

    • Utilized C6 rat glioma cell line for experiments.
    • Measured insulin binding to intact cell monolayers.
    • Assessed the impact of dexamethasone, corticosterone, and 17 alpha-methyltestosterone on insulin binding.

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  • Investigated the role of protein synthesis using cycloheximide.

    • Main Results:

    • Dexamethasone decreased insulin binding in a dose- and time-dependent manner (maximal effect at 48-72h with 50 nM).
    • Glucocorticoids reduced the total number of binding sites and increased the dissociation constant (Kd) of the low-affinity site.
    • Cycloheximide increased insulin binding, indicating receptor accumulation in the absence of protein synthesis.
    • Cycloheximide blocked dexamethasone's effect, suggesting protein synthesis is necessary for glucocorticoid action.
    • Pretreatment with dexamethasone prevented cycloheximide-induced receptor increase, indicating depletion of total cellular receptors.

    Conclusions:

    • Glucocorticoids significantly downregulate insulin receptors in C6 rat glioma cells.
    • Protein synthesis is essential for the glucocorticoid-induced reduction of insulin receptors.
    • Glucocorticoids appear to deplete both cell surface and total cellular insulin receptors.