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Related Experiment Videos

Effect of cycloheximide on corticosteroid-induced changes in colonic function.

A N Charney, J D Wallach, M Donowitz

    The American Journal of Physiology
    |August 1, 1982
    PubMed
    Summary

    Chronic steroid treatment affects colon absorption. Protein synthesis inhibition by cycloheximide blocked mineralocorticoid effects but only partially glucocorticoid effects, suggesting different mechanisms for these hormones.

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    Physiological genomics·2011

    Area of Science:

    • Gastroenterology
    • Endocrinology
    • Molecular Biology

    Background:

    • Corticosteroids, including mineralocorticoids and glucocorticoids, influence colonic function.
    • Chronic administration of these hormones increases sodium and water absorption and Na-K-ATPase activity in the colon.

    Purpose of the Study:

    • To investigate the distinct mechanisms of action for mineralocorticoids and glucocorticoids in the colon.
    • To determine the role of protein synthesis in mediating corticosteroid-induced colonic changes.

    Main Methods:

    • Rats were treated with cycloheximide (protein synthesis inhibitor), deoxycorticosterone (DOCA, a mineralocorticoid), methylprednisolone (MP, a glucocorticoid), or combinations thereof.
    • Colonic water absorption, transmural potential difference, and Na-K-ATPase activity were measured.

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    Main Results:

    • Cycloheximide alone increased transmural potential difference but did not affect absorption or Na-K-ATPase activity.
    • Cycloheximide completely blocked DOCA-induced increases in colonic absorption and Na-K-ATPase activity.
    • Cycloheximide blocked Na-K-ATPase increases from MP but only partially reduced MP-induced absorption increases.

    Conclusions:

    • The results suggest that Na-K-ATPase is a primary mediator for mineralocorticoid action in the colon.
    • Glucocorticoid action on colonic absorption may involve pathways independent of Na-K-ATPase upregulation.
    • Further research is needed to clarify the precise role of Na-K-ATPase in maximal glucocorticoid response.