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Role of Insulin Resistance in Human Disease

  • Chapter
Multiple Risk Factors in Cardiovascular Disease

Part of the book series: Medical Science Symposia Series ((MSSS,volume 1))

Abstract

The ability of insulin to stimulate glucose uptake can vary substantially in non-obese individuals with no apparent disease (10). In addition, differences in either degree of obesity or level of habitual physical activity can also modulate in vivo insulin action (18,24). In an apparent attempt to maintain glucose homeostasis, the compensatory response to a decrease in insulin-stimulated glucose up take is an increase in plasma insulin concentration. A defect in the ability of insulin-stimulated glucose uptake has also been demonstrated (21) in patients with either impaired glucose tolerance (IGT) or non-insulin dependent diabetes mellitus (NIDDM). It has been suggested that the degree to which glucose tolerance deteriorates in these individuals is a function of the level of compensatory hyperinsulinemia that they can maintain, and the appearance of severe fasting hyperglycemia marks the failure of the pancreatic beta cell to sustain the necessary increase in insulin secretory response (21).

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Authors
  1. Gerald M. Reaven M.D.
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Editor information

Editors and Affiliations

  1. Baylor College of Medicine and The Methodist Hospital, Houston, Texas, USA

    Antonio M. Gotto Jr.

  2. National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, USA

    Claude Lenfant

  3. Institute of Pharmacological Sciences, University of Milan, Milan, Italy

    Rodolfo Paoletti  & Maurizio Soma (Assistant Editor) &  (Assistant Editor)

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© 1992 Springer Science+Business Media Dordrecht

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Reaven, G.M. (1992). Role of Insulin Resistance in Human Disease. In: Gotto, A.M., Lenfant, C., Paoletti, R., Soma, M. (eds) Multiple Risk Factors in Cardiovascular Disease. Medical Science Symposia Series, vol 1. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-2700-4_10

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  • DOI: https://doi.org/10.1007/978-94-011-2700-4_10

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-5196-5

  • Online ISBN: 978-94-011-2700-4

  • eBook Packages: Springer Book Archive

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