Hypercholesterolemia, Hypocholesterolemia, Hypertriglyceridemia, in Vivo Kinetics

  • Claude L. Malmendier
  • P. Alaupovic
  • H. Bryan BrewerJr.

Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 285)

Table of contents

  1. Front Matter
    Pages i-x
  2. Cholesterol Metabolism

    1. Front Matter
      Pages xi-xi
    2. Vassilis I. Zannis, Dimitris Kardassis, Kinya Ogami, Margarita Hadzopoulou-Cladaras, Christos Cladaras
      Pages 1-23
    3. Thomas L. Innerarity, Kristina Boström
      Pages 25-31
    4. Katriina Aalto-Setälä, Kimmo Kontula
      Pages 33-37
    5. P. J. Barter, L. B. F. Chang, O. V. Rajaram
      Pages 59-64
    6. Steven J. Busch, Gary A. Martin, Roger L. Barnhart, Margaret A. Flanagan, Richard L. Jackson
      Pages 65-69
    7. Yves L. Marcel, Alan R. Tall, Mireille Hogue, Ross W. Milne, Ruth McPherson
      Pages 77-80
    8. E. L. Bierman, J. Oram, A. Mendez
      Pages 81-83
    9. Ronald Barbaras, Pascal Puchois, Anne Pradines Figuères, Armin Steinmetz, Véronique Clavey, Nordine Ghalim et al.
      Pages 85-92
    10. Nicolas Duverger, Nordine Ghalim, Nathalie Theret, Philippe Duchateau, Gustave Aguie, Gérard Ailhaud et al.
      Pages 93-99
    11. L. Lagrost, P. Gambert, A. Athias, C. Lallemant
      Pages 109-115
    12. G. M. Anantharamaiah, C. G. Brouillette, J. A. Engler, H. De Loof, Y. V. Venkatachalapathi, J. Boogaerts et al.
      Pages 131-140
    13. J-L. De Coen, J-P. Kocher, C. Delcroix, J-F. Lontie, C. L. Malmendier
      Pages 141-145

About this book


The past two decades have seen steady progress in our understanding of the pathogenesis of atherosclerosis. The role of low density lipoprotein (LOL) increase and of LOL receptor deficiency or malfunctions in familial hypercholesterolemia has been largely enlightened by the works of Brown and Goldstein. These authors postulated also that modification of LOL to a form recognized by the scavenger or acetyl-LOL receptor may be required for lipid loading of macrophage-derived foam cells in the lesions. A growing body of evidence suggests that oxidative modification of LOL could enhance its atherogenicity by its implication as a factor in the generation of foam cells. Thus, if the role of LOL in the pathogenesis of hypercholesterolemia was well established a great deal of information appears currently on new approaches such as the mechanisms leading to the accumulation of foam cells, the impact of LOL structural alterations, notably oxidation and the role of gene mutations of apolipoprotein Band/or LOL receptor The opening topic is devoted to these new avenues outlined in the field of hypercholesterolemia. The first part concerns the genetic aspects of atherosclerosis: mainly the genetics of apo 1 ipoprote ins , their transcriptional regulation, the amino acid mutations of the apo B gene and of the LOL receptor gene, the structural domains and the acylation sites of apoprotein B.


Amino acid Lipid Oxidation genes genetics metabolism proteins transcription

Editors and affiliations

  • Claude L. Malmendier
    • 1
  • P. Alaupovic
    • 2
  • H. Bryan BrewerJr.
    • 3
  1. 1.Research Foundation on AtherosclerosisBrusselsBelgium
  2. 2.Lipoprotein and Atherosclerosis Resaerch ProgramOklahoma Medical Research FoundationOklahoma CityUSA
  3. 3.Molecular Disease Branch, National Heart, Lung, and Blood InstituteNational Institutes of HealthBethesdaUSA

Bibliographic information

  • DOI https://doi.org/10.1007/978-1-4684-5904-3
  • Copyright Information Springer-Verlag US 1991
  • Publisher Name Springer, Boston, MA
  • eBook Packages Springer Book Archive
  • Print ISBN 978-1-4684-5906-7
  • Online ISBN 978-1-4684-5904-3
  • Series Print ISSN 0065-2598
  • About this book