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Are insulin receptors clinically significant?

H S Seltzer

    The Journal of Laboratory and Clinical Medicine
    |December 1, 1982
    PubMed
    Summary

    Type I diabetes results from beta-cell failure, while Type II diabetes involves insulin resistance and deficiency. Understanding post-receptor defects is key, suggesting insulin

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    Area of Science:

    • Endocrinology
    • Metabolic Disorders

    Background:

    • Clinical diabetes mellitus pathophysiology was largely understood prior to the discovery of insulin receptors.
    • Type I diabetes (growth-onset) is characterized by primary beta-cell failure with normal insulin sensitivity and receptor levels.
    • Type II diabetes (adult-onset) involves a combination of insulin deficiency and resistance, leading to hyperinsulinemia.

    Purpose of the Study:

    • To elucidate the roles of insulin receptors and post-receptor defects in different types of diabetes mellitus.
    • To re-evaluate the significance of the insulin hormone versus its receptor in diabetes pathogenesis.

    Main Methods:

    • Review and synthesis of existing knowledge on diabetes mellitus pathophysiology.
    • Analysis of the relationship between beta-cell function, insulin sensitivity, insulin receptor concentration, and clinical presentation in Type I and Type II diabetes.

    Main Results:

    • Type I diabetes is primarily a beta-cell defect, independent of insulin receptor abnormalities.
    • Type II diabetes exhibits secondary downregulation of insulin receptors due to chronic hyperinsulinemia.
    • Obesity exacerbates hyperinsulinemia in Type II diabetes but insulin levels decrease as the disease progresses.

    Conclusions:

    • Post-receptor defects in glucose transport and intracellular insulin action are critical and linked to impaired insulin secretion.
    • The insulin hormone itself plays a more central role in diabetes than its receptor.
    • Further research is needed to fully understand post-receptor signaling pathways and their relation to insulin secretion defects.

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