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Volume 271, Number 32, Issue of August 9, 1996 pp. 19058-19065
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

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Opposite Effects of Cholesteryl Ester Transfer Protein and Phospholipid Transfer Protein on the Size Distribution of Plasma High Density Lipoproteins
PHYSIOLOGICAL RELEVANCE IN ALCOHOLIC PATIENTS

(Received for publication, March 25, 1996, and in revised form, May 15, 1996)

Laurent Lagrost , Anne Athias , Bernard Herbeth ^¶ , Valérie Guyard-Dangremont , Yves Artur , François Paille ^'' , Philippe Gambert and Christian Lallemant

From the  Laboratoire de Biochimie des Lipoprotéines, INSERM CJF 93-10, Faculté de Médecine, 21033 Dijon, France, the ^¶ Laboratoire du Centre de Médecine Préventive, CNRS URA 597, 54500 Vandoeuvre-lès-Nancy, France, the  Formation de Biochimie Pharmacologique, Faculté de Médecine et de Pharmacie, 21033 Dijon, France, and the ^'' Centre d'Alcoologie, Centre Hospitalier Régional Universitaire, Hôpital Fournier, 54000 Nancy, France

The aim of the present study was to investigate the role of the cholesteryl ester transfer protein (CETP) and the phospholipid transfer protein (PLTP) in determining the size distribution of high density lipoproteins (HDL) in human plasma. Whereas both purified CETP and PLTP preparations were able to promote the size redistribution of isolated HDL₃, CETP favored the emergence of small HDL, while PLTP induced the formation of both small and large conversion products. When the total plasma lipoprotein fractions isolated from nine distinct subjects were incubated for 24 h at 37 °C with either purified PLTP or purified CETP, significant alterations in the relative proportions of the five distinct plasma HDL subpopulations, i.e., HDL_2b (9.71-12.90 nm), HDL_2a (8.77-9.71 nm), HDL_3a (8.17-8.77 nm), HDL_3b (7.76-8.17 nm), and HDL_3c (7.21-7.76 nm) were also observed. PLTP induced a significant increase in the relative abundance of HDL_2b (8.66 ± 2.34% versus 7.87 ± 1.83% in controls; p < 0.01) and a significant decrease in the relative abundance of HDL_3a (32.76 ± 3.42% versus 37.87 ± 2.62% in controls; p < 0.05). In contrast, CETP significantly reduced the relative proportion of HDL_2a (33.03 ± 2.53% versus 37.56 ± 6.43% in controls; p < 0.01) but significantly increased the relative proportion of both HDL_3b (21.36 ± 6.97% versus 15.58 ± 7.75% in controls; p < 0.01) and HDL_3c (3.21 ± 4.84% versus 1.13 ± 0.56% in controls; p < 0.05). Finally, in order to assess further the physiological relevance of in vitro observations, CETP activity, PLTP activity, and HDL size distribution were determined in plasmas from 33 alcoholic patients entering a cessation program. Alcohol withdrawal was associated with (i) a significant increase in plasma CETP activity (173.5 ± 70.5%/h/ml before versus 223.2 ± 69.3%/h/ml after alcohol withdrawal, p = 0.0007), (ii) a significant reduction in plasma PLTP activity (473.9 ± 203.7%/h/ml before versus 312.7 ± 148.4%/h/ml after alcohol withdrawal, p = 0.0001), and (iii) a significant shift of large HDL_2b and HDL_2a toward small HDL_3b and HDL_3c. On the one hand, changes in plasma CETP activity correlated negatively with changes in the proportion of HDL_2a (r = 0.597, p = 0.0002) and positively with changes in the proportion of HDL_3b (r = 0.457, p = 0.0075). On the other hand, changes in plasma PLTP activity correlated positively with changes in the proportion of HDL_2b (r = 0.482, p = 0.0045) and negatively with changes in the proportion of HDL_3a (r = 0.418, p = 0.0154). Taken together, data of the present study revealed that plasma PLTP and CETP can exert opposite effects on the size distribution of plasma HDL. PLTP can promote the formation of HDL_2b particles at the expense of HDL_3a, while CETP can promote the formation of HDL_3b particles at the expense of HDL_2a.

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