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Research Article Free access | 10.1172/JCI114764

Accumulation of apolipoprotein E-rich high density lipoproteins in hyperalphalipoproteinemic human subjects with plasma cholesteryl ester transfer protein deficiency.

S Yamashita, D L Sprecher, N Sakai, Y Matsuzawa, S Tarui, and D Y Hui

Department of Pathology, College of Medicine, University of Cincinnati, Ohio 45267-0529.

Find articles by Yamashita, S. in: PubMed | Google Scholar

Department of Pathology, College of Medicine, University of Cincinnati, Ohio 45267-0529.

Find articles by Sprecher, D. in: PubMed | Google Scholar

Department of Pathology, College of Medicine, University of Cincinnati, Ohio 45267-0529.

Find articles by Sakai, N. in: PubMed | Google Scholar

Department of Pathology, College of Medicine, University of Cincinnati, Ohio 45267-0529.

Find articles by Matsuzawa, Y. in: PubMed | Google Scholar

Department of Pathology, College of Medicine, University of Cincinnati, Ohio 45267-0529.

Find articles by Tarui, S. in: PubMed | Google Scholar

Department of Pathology, College of Medicine, University of Cincinnati, Ohio 45267-0529.

Find articles by Hui, D. in: PubMed | Google Scholar

Published September 1, 1990 - More info

Published in Volume 86, Issue 3 on September 1, 1990
J Clin Invest. 1990;86(3):688–695. https://doi.org/10.1172/JCI114764.
© 1990 The American Society for Clinical Investigation
Published September 1, 1990 - Version history
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Abstract

This study characterized the plasma lipoproteins of familial hyperalphalipoproteinemic patients with or without deficiency of cholesteryl ester transfer protein (CETP) activity. The subjects with CETP deficiency have increased levels of apolipoprotein (apo) E. The increased concentration of apo E in these subjects was correlated to the appearance of apo E-rich high density lipoproteins (HDL). Sodium dodecyl sulfate-polyacrylamide gel analysis revealed that these lipoproteins contained predominantly the apo E (82%) and little amount of apo A-I (18%). These apo E-rich HDL displayed a much higher affinity than human LDL in binding to LDL receptors on human fibroblasts. Furthermore, 3.5 times fewer apo E-rich HDL than LDL were required to saturate the receptors on fibroblasts. These data indicated that the apo E-rich HDL in CETP-deficient human subjects contained multiple copies of apo E and bound to the LDL receptor through multiple interactions. The apo E-rich HDL, with similar properties as cholesterol-induced apo E HDLc, were not detectable in normal human subjects or in hyperalphalipoproteinemic subjects with normal CETP activity. The apo E-containing HDL in the latter subjects were smaller and contained only small amounts of apo E (14%). The difference in apo E-containing HDL in these subjects suggests a correlation between CETP level and the appearance of apo E-rich HDL.

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