Chapter 4. Regulation of Cell Cholesterol Content

  1. Ruth Porter and
  2. Julie Knight
  1. J. Martyn Bailey

Published Online: 30 MAY 2008

DOI: 10.1002/9780470719954.ch4

Ciba Foundation Symposium 12 - Atherogenesis: Initiating Factors

Ciba Foundation Symposium 12 - Atherogenesis: Initiating Factors

How to Cite

Bailey, J. M. (1973) Regulation of Cell Cholesterol Content, in Ciba Foundation Symposium 12 - Atherogenesis: Initiating Factors (eds R. Porter and J. Knight), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/9780470719954.ch4

Author Information

  1. Biochemistry Department, George Washington University School of Medicine, Washington, D.C.

Publication History

  1. Published Online: 30 MAY 2008
  2. Published Print: 1 JAN 1973

ISBN Information

Print ISBN: 9789021940137

Online ISBN: 9780470719954



  • cholesterol;
  • lipids;
  • cells;
  • atherosclerotic plaque;
  • serum lipoproteins


The accumulation of cholesterol and other lipids by cells in the intima of thoracic aorta is observed in the very early stages of atherosclerosis. Degeneration of lipid-laden cells contributes to the tissue lipid pool, and together with the associated inflammatory response is a potentiating factor in the formation of the atherosclerotic plaque. The conditions affecting cholesterol uptake have been studied in tissue culture using cells growing in [14C]cholesterol-labelled sera from normal and atherosclerotic subjects. Cholesterol accumulation is the resultant of three processes: transport into cells, excretion from cells, and cke tiovo synthesis, principally from glucose and acetate. Transport is controlled externally by the serum lipoproteins, and the internal cholesterol level regulates synthesis by a feedback inhibition mechanism. Cholesterol entry involves uptake by sterol receptors in the cell membrane, followed by slow transfer to intracellular cholesterol carriers. Intact serum lipoproteins do not appear to enter to any significant extent. There is evidence that soluble intracellular cholesterol carriers may regulate cholesterol biosynthesis. Cholesterol esters are taken up intact and, after hydrolysis, are usually deposited largely as free cholesterol. Serum lipoproteins also stimulate the excretion of intracellularly synthesized cholesterol. Cholesterol accumulation in cells is determined largely by the balance between uptake, excretion and biosynthesis and controlled by the degree of saturation of the lipoprotein carriers. The regulation of cell cholesterol content is thus revealed as a dynamic process involving continuous interaction of the cellular biosynthetic pathways with the lipoprotein mediated transport into and out of the cell.