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The insulin receptor.

K R Lyen

    Annals of the Academy of Medicine, Singapore
    |April 1, 1985
    PubMed
    Summary
    This summary is machine-generated.

    The insulin receptor, a glycoprotein, exhibits tissue-specific distribution and undergoes internalization and recycling. Its alterations are linked to insulin resistance in obesity and type II diabetes.

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    Area of Science:

    • Biochemistry
    • Cell Biology
    • Endocrinology

    Background:

    • The insulin receptor is a crucial glycoprotein mediating insulin's effects.
    • Its structure involves subunits linked by disulfide bonds and exhibits tissue-specific distribution.
    • Receptor localization varies, with liver plasma membranes showing single receptors and adipocytes displaying grouped receptors.

    Purpose of the Study:

    • To elucidate the structural and functional characteristics of the insulin receptor.
    • To investigate the role of insulin receptor alterations in insulin resistance and diabetes.
    • To understand the impact of physiological states and external factors on insulin receptor binding.

    Main Methods:

    • Analysis of insulin receptor structure and subunit composition.

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  • Investigation of receptor distribution in different cell types (liver, adipocytes, fibroblasts).
  • Examination of insulin receptor internalization, degradation, and recycling processes.

    • Main Results:

    • Insulin receptors are glycoproteins (approx. 300,000 MW) with distinct subunit arrangements and tissue-specific localization.
    • Receptor groups in adipocytes are stabilized by disulfide bonds distinct from subunit linkages.
    • Insulin binding triggers receptor internalization via pinocytosis or coated pits, followed by lysosomal degradation or recycling.

    Conclusions:

    • Reduced insulin receptor numbers and post-receptor defects contribute to insulin resistance in obesity and type II diabetes.
    • Physiological states like fasting, exercise, and pregnancy modulate insulin receptor binding.
    • Glucocorticoids may induce post-receptor insulin resistance, and auto-antibodies to the receptor cause severe insulin resistance.