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Effects of glucocorticoids on peptide chain initiation in heart and skeletal muscle

D E Rannels, S R Rannels, J B Li

    Advances in Myocardiology
    |January 1, 1980
    PubMed

    Insights

    Cortisone acetate significantly reduced skeletal muscle protein synthesis by inhibiting peptide-chain initiation and decreasing RNA. Heart muscle protein synthesis remained unaffected by the hormone treatment.

    Area of Science:

    • Biochemistry
    • Molecular Biology
    • Endocrinology

    Background:

    • Glucocorticoids are known to affect protein metabolism.
    • Skeletal muscle and heart muscle exhibit differential responses to hormonal stimuli.
    • Protein synthesis regulation involves complex mechanisms including initiation factors.

    Purpose of the Study:

    • To investigate the impact of glucocorticoids on protein synthesis in different rat tissues.
    • To elucidate the role of RNA content and peptide-chain initiation in glucocorticoid-induced changes in protein synthesis.
    • To explore the relationship between initiation factor activity and tissue RNA content.

    Main Methods:

    • Treatment of rats with cortisone acetate and dexamethasone.
    • Measurement of skeletal muscle and heart protein synthesis rates.
    • Analysis of tissue RNA content and peptide-chain initiation.
    • Assay of initiation factor (eIF-2) activity in muscle tissues.

    Main Results:

    • Cortisone acetate reduced skeletal muscle protein synthesis by 56% due to decreased RNA and inhibited peptide-chain initiation.
    • Heart muscle protein synthesis was unaffected by cortisone acetate.
    • Dexamethasone inhibited peptide-chain initiation in skeletal muscle without altering RNA or initiation factor activity.
    • A correlation was observed between initiation factor activity and tissue RNA content.

    Conclusions:

    • Glucocorticoids differentially regulate protein synthesis in skeletal and heart muscle.
    • Inhibition of peptide-chain initiation and reduction in RNA are key mechanisms for glucocorticoid-induced muscle protein catabolism.
    • Further investigation into the purification of eIF-2 is needed to understand glucocorticoid mechanisms.

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