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Effect of acute hyperglycemia on potassium (86Rb+) permeability and plasma lipid peroxidation in subjects with normal glucose tolerance

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Abstract

Hyperglycemia is likely to be one of the important determinants of ion transport as it is known to induce oxidative stress and may thus enhance non-specific permeability of membranes. The aim of the present study was to evaluate the effects of an acute increase in glycemia on 86Rb+ (a marker for K+) influx and lipid peroxidation. We evaluated the 75-g oral glucose tolerance test (OGTT)-induced modification on 86Rb+ influx and plasma lipid peroxidation in 20 subjects with normal glucose tolerance (NGT). After 2-hour glucose loading, the levels of passive 86Rb+ influx and plasma lipid peroxidation were significantly increased, whereas the active influx of 86Rb+ was unchanged. The total and passive influx of 86Rb+ into erythrocytes was significantly correlated with the level of plasma lipid peroxidation. This study demonstrates that acute hyperglycemia induces an increase in the passive influx of 86Rb+ in subjects with NGT, suggesting that acute hyperglycemia may produce an oxidative stress in plasma. These changes may be among the earliest changes occurring in response to hyperglycemia.

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Authors and Affiliations

  1. Department of Medical Biology Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey

    Mehmet Güven, I. Onaran & G. Sultuybek

  2. Department of Genetic and Teratology Research Center (GETAM), Division of Biomedical Sciences Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey

    T. Ulutin

  3. Department of Internal Medicine, Division of Endocrinology and Metabolism, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey

    H. Hatemi

Authors
  1. Mehmet Güven
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  2. I. Onaran
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  3. T. Ulutin
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  4. G. Sultuybek
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  5. H. Hatemi
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Correspondence to Mehmet Güven.

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Güven, M., Onaran, I., Ulutin, T. et al. Effect of acute hyperglycemia on potassium (86Rb+) permeability and plasma lipid peroxidation in subjects with normal glucose tolerance. J Endocrinol Invest 24, 231–235 (2001). https://doi.org/10.1007/BF03343852

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