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Pancreatic endocrine function in cortisol-treated thyroidectomized calves

S R Bloom, A V Edwards, A S Fielding

    The Journal of Physiology
    |September 1, 1981
    PubMed
    Summary
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    Cortisol-induced diabetes in calves stems from impaired insulin release, affecting pancreatic glucagon and polypeptide. Thyroxine treatment reversed these diabetic signs and restored normal insulin function.

    Area of Science:

    • Endocrinology
    • Metabolic Research
    • Animal Models

    Background:

    • Thyroidectomy and exogenous cortisol administration can induce diabetic syndromes in animals.
    • Pancreatic endocrine hormones, including insulin, glucagon, and pancreatic polypeptide (PP), play crucial roles in glucose homeostasis.
    • Understanding the interplay between thyroid status, cortisol, and pancreatic hormones is vital for metabolic research.

    Purpose of the Study:

    • To investigate the effects of cortisol-induced diabetes on pancreatic endocrine function in thyroidectomized calves.
    • To determine the role of thyroxine in reversing the diabetic state and associated hormonal changes.
    • To elucidate the primary defect leading to diabetes and the consequential alterations in pancreatic hormone release.

    Main Methods:

    Related Experiment Videos

  • Induction of a diabetic syndrome in thyroidectomized calves using exogenous cortisol.
  • Monitoring of plasma concentrations of insulin, glucagon, and pancreatic polypeptide (PP).
  • Administration of thyroxine to assess its reversal effects on the diabetic syndrome and hormonal levels.
  • Evaluation of neurally mediated insulin release in response to 2-deoxyglucose.
  • Assessment of starvation as a therapeutic intervention for reducing glucose and glucagon levels.

    • Main Results:

    • Cortisol-induced diabetes was associated with decreased plasma insulin concentrations.
    • Significant increases in post-absorptive plasma concentrations of pancreatic glucagon and PP were observed in diabetic calves.
    • Thyroxine administration reversed the diabetic syndrome, normalizing plasma glucose and restoring pancreatic endocrine function.
    • Starvation effectively reduced plasma glucose and glucagon but did not affect insulin or PP levels.
    • Neurally mediated insulin release was impaired in diabetic calves and recovered with thyroxine treatment, while glucagon and PP release remained unaffected.

    Conclusions:

    • The primary defect in cortisol-induced diabetes in these calves is a failure of insulin release.
    • Consequential changes in the release rates of pancreatic glucagon and PP are associated with this primary defect.
    • Thyroxine plays a critical role in reversing the diabetic state by restoring normal insulin release and overall pancreatic endocrine function.