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Related Experiment Videos

Glucocorticoids decrease in conversion of thyroxine into 3, 5, 3'-tri-iodothyronine by isolated rat renal tubules

P Heyma, R G Larkins

    Clinical Science (London, England : 1979)
    |February 1, 1982
    PubMed
    Summary

    Glucocorticoids directly regulate thyroid hormone levels by inhibiting the conversion of thyroxine (T4) to tri-iodothyronine (T3) in rat kidneys. This finding suggests glucocorticoids play a key role in controlling T3 production and T4 deiodination.

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    Area of Science:

    • Endocrinology
    • Molecular Biology
    • Renal Physiology

    Background:

    • Thyroid hormones, including thyroxine (T4) and tri-iodothyronine (T3), are crucial for metabolic regulation.
    • Glucocorticoids are steroid hormones with diverse physiological effects, including modulation of gene expression.
    • The deiodination of T4 to T3 is a key step in thyroid hormone activation and metabolism.

    Purpose of the Study:

    • To investigate the direct effect of glucocorticoids on the deiodination of T4 to T3 in rat renal tubules.
    • To elucidate the mechanism underlying glucocorticoid-mediated inhibition of T4 to T3 conversion.

    Main Methods:

    • Preparation of rat renal tubules using collagenase digestion.
    • Short-term (6h) and long-term (16h) incubation experiments with varying concentrations of glucocorticoids (cortisol, dexamethasone, corticosterone).

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  • Assessment of T4 to T3 conversion rates and the effects of actinomycin D and progesterone.

    • Main Results:

    • Cortisol and dexamethasone inhibited T4 to T3 conversion in a time-dependent manner.
    • Inhibition was observed at concentrations of 2 X 10-4 mol/l (cortisol) and 2 X 10-5 mol/l (dexamethasone) in short-term experiments.
    • Long-term experiments showed inhibition at 1 X 10-12 mol/l and above, with physiological corticosterone (1 X 10-8 mol/l) also decreasing T3 generation.
    • Inhibition was prevented by actinomycin D and progesterone, indicating a nuclear transcription-dependent mechanism.

    Conclusions:

    • Physiological concentrations of glucocorticoids directly impact T3 production from T4 in rat renal tubules.
    • Glucocorticoids may serve as significant regulators of T4 deiodination and subsequent thyroid hormone activity.
    • The mechanism involves glucocorticoid receptor binding and effects on nuclear transcription.