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Related Experiment Video

Updated: Nov 21, 2025

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test OGTT and Insulin Tolerance Test ITT
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Mechanism of the postreceptor defect in insulin action in human obesity. Decrease in glucose transport system

T P Ciaraldi, O G Kolterman, J M Olefsky

    The Journal of Clinical Investigation
    |October 1, 1981
    PubMed
    Summary
    This summary is machine-generated.

    Obese patients show impaired insulin action due to reduced glucose transport activity. This study links decreased adipocyte insulin receptors and post-receptor defects to insulin resistance in obesity.

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    Area of Science:

    • Metabolic disorders
    • Cellular physiology
    • Endocrinology

    Background:

    • Obesity is frequently associated with insulin resistance.
    • Insulin resistance impairs glucose uptake in peripheral tissues, particularly adipose tissue.
    • The precise mechanisms underlying insulin resistance in obesity are not fully elucidated.

    Purpose of the Study:

    • To investigate insulin-stimulated glucose transport in isolated adipocytes from normal and obese individuals.
    • To determine the relationship between adipocyte insulin receptors and glucose transport function in obesity.
    • To identify potential post-receptor defects in insulin action in obese patients.

    Main Methods:

    • Isolated adipocytes were prepared from 10 normal and 11 obese individuals.
    • Insulin-stimulated 3-O-methyl glucose transport was measured.
    • Dose-response curves for insulin and glucose transport were analyzed.
    • Adipocyte insulin receptor levels were assessed.
    • In vivo glucose clamp studies were performed for comparison.

    Main Results:

    • Obese individuals exhibited a rightward shift in insulin-glucose transport dose-response curves.
    • This shift correlated significantly with reduced adipocyte insulin receptors (r = 0.48, P < 0.01).
    • Eight out of eleven obese patients showed decreased basal and maximal glucose transport rates, indicating a post-receptor defect.
    • Three obese patients had a rightward shift without a decrease in maximal insulin effect, consistent with normal glucose disposal.

    Conclusions:

    • The mechanism of post-receptor insulin resistance in many obese patients involves decreased activity of the glucose transport effector system.
    • Reduced adipocyte insulin receptors contribute to impaired insulin sensitivity in obesity.
    • These findings highlight the complex nature of insulin resistance in obesity, involving both receptor and post-receptor defects.