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Diabetes 53:2633-2639, 2004
© 2004 by the American Diabetes Association, Inc.

Alterations in Plasma Vitamin E Distribution in Type 2 Diabetic Patients With Elevated Plasma Phospholipid Transfer Protein Activity

Martina Schneider1, Bruno Vergès2, Alexis Klein1, Elizabeth R. Miller3, Valérie Deckert1, Catherine Desrumaux1, David Masson1, Philippe Gambert1, Jean-Marcel Brun2, Jamila Fruchart-Najib4, Denis Blache1, Joseph L. Witztum3, and Laurent Lagrost1

1 Institut National de la Santé et de la Recherche Médicale (INSERM) U498, Dijon, France
2 Department of Endocrinology and Diabetes, Bocage Hospital, Dijon, France
3 Department of Medicine, University of California, San Diego, La Jolla, California
4 INSERM U545, Pasteur Institute, Lille, France

Mouse studies indicated that plasma phospholipid transfer protein (PLTP) determines the plasma distribution of vitamin E, a potent lipophilic antioxidant. Vitamin E distribution, antioxidant status, and titer of anti–oxidized LDLs (oxLDL) autoantibodies were evaluated in plasma from control subjects (n = 31) and type 2 diabetic patients (n = 31) with elevated plasma PLTP concentration. Unlike diabetic and control HDLs, which displayed similar vitamin E contents, diabetic VLDLs and diabetic LDLs contained fewer vitamin E molecules than normal counterparts. Plasma PLTP concentration in diabetic plasmas correlated negatively with vitamin E in VLDL+LDL, but positively with vitamin E in HDL, with an even stronger correlation with the VLDL+LDL–to–HDL vitamin E ratio. Circulating levels of oxLDL were significantly higher in diabetic plasmas than in control plasmas. Whereas the titer of IgG autoantibodies to modified LDL did not differ significantly between diabetic patients and control subjects, diabetic plasmas showed significantly lower levels of potentially protective IgM autoantibodies. The present observations support a pathophysiological role of PLTP in decreasing the vitamin E content of apolipoprotein B–containing lipoproteins, but not of HDL in plasma of type 2 diabetic patients, contributing to a greater potential for LDL oxidation.

Address correspondence and reprint requests to Laurent Lagrost, INSERM U498, Laboratoire de Biochimie des Lipoprotéines, Faculté de Médecine, BP 87900, 21079 Dijon Cedex, France. E-mail: laurent.lagrost{at}u-bourgogne.fr


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Copyright © 2004 by the American Diabetes Association.