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Cyclic nucleotide phosphodiesterases and thyroid hormones.

R G Van Inwegen, G A Robison, W J Thompson

    The Journal of Biological Chemistry
    |April 10, 1975
    PubMed
    Summary
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    Thyroid hormones regulate fat cell responsiveness by modulating cyclic AMP phosphodiesterase activity. In hypothyroidism, elevated enzyme activity reduces lipolytic response, which is restored by triiodothyronine treatment.

    Area of Science:

    • Endocrinology
    • Cellular Biology
    • Metabolism

    Background:

    • Thyroid hormones play a crucial role in regulating cellular metabolism and responsiveness to various stimuli.
    • Cyclic adenosine 3':5'-monophosphate (cyclic AMP) is a key second messenger involved in lipolysis in adipocytes.
    • Dysregulation of cyclic AMP metabolism can lead to metabolic disorders, including altered fat cell responsiveness.

    Purpose of the Study:

    • To investigate the role of thyroid hormones in regulating the activity of cyclic adenosine 3':5'-monophosphate (cyclic AMP) phosphodiesterase in rat epididymal adipocytes.
    • To determine if modulation of phosphodiesterase activity by thyroid hormones affects adipocyte responsiveness to lipolytic agents.
    • To elucidate the mechanism by which hypothyroidism impacts adipocyte lipolysis at the enzymatic level.

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    Main Methods:

    • Induction of hypothyroidism in rats using propylthiouracil.
    • Measurement of adipocyte responsiveness to lipolytic agents (epinephrine, glucagon).
    • Assay of particulate low K-m and soluble high K-m cyclic AMP phosphodiesterase activity.
    • In vivo administration of triiodothyronine to hypothyroid rats.
    • Assessment of protein kinase activity and forms in adipocytes.

    Main Results:

    • Hypothyroid rat adipocytes showed unresponsiveness to lipolytic agents, correlating with elevated V-max of particulate low K-m cyclic AMP phosphodiesterase.
    • In vivo triiodothyronine treatment normalized both adipocyte lipolytic response and phosphodiesterase V-max.
    • No correlation was found between thyroid status and soluble high K-m cyclic AMP phosphodiesterase activity.
    • Hypothyroid adipocytes exhibited a shift in protein kinase equilibrium, with less cyclic AMP-independent form, consistent with increased phosphodiesterase activity.

    Conclusions:

    • Modulation of particulate low K-m cyclic AMP phosphodiesterase by thyroid hormones is a key mechanism regulating adipocyte lipolytic responsiveness.
    • Increased phosphodiesterase activity in hypothyroidism leads to a reduced cyclic AMP pool, impairing lipolysis.
    • Thyroid hormone replacement therapy can restore normal adipocyte function by normalizing phosphodiesterase activity.