Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1986;74:805-814

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Meddings, J. B.
Right arrow Articles by Dietschy, J. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Meddings, J. B.
Right arrow Articles by Dietschy, J. M.

Circulation, Vol 74, 805-814, Copyright © 1986 by American Heart Association


ARTICLES

Regulation of plasma levels of low-density lipoprotein cholesterol: interpretation of data on low-density lipoprotein turnover in man

JB Meddings and JM Dietschy

At the present time the most useful technique with which to examine the kinetics of low-density lipoprotein (LDL) cholesterol in vivo is the labeled LDL turnover study. However, a major limitation of this method is that, despite its ability to accurately measure both the plasma LDL concentration and LDL production rate, it cannot directly quantify LDL receptor activity. The present study defines the equations that describe the relationship between LDL cholesterol production rate, LDL receptor number, and plasma LDL cholesterol concentration. These equations provide a method that allows calculation of total LDL receptor activity based on the results of an LDL turnover study. With the use of this technique and data from previously published series, the effects of the genetic absence of receptors, aging, and the treatment of hypercholesterolemia with mevinolin on LDL cholesterol kinetics were analyzed.


This article has been cited by other articles:


Home page
J. Clin. Endocrinol. Metab.Home page
E. R. Christ, M. H. Cummings, N. Jackson, M. Stolinski, P. J. Lumb, A. S. Wierzbicki, P. H. Sonksen, D. L. Russell-Jones, and A. M. Umpleby
Effects of Growth Hormone (GH) Replacement Therapy on Low-Density Lipoprotein Apolipoprotein B100 Kinetics in Adult Patients with GH Deficiency: A Stable Isotope Study
J. Clin. Endocrinol. Metab., April 1, 2004; 89(4): 1801 - 1807.
[Abstract] [Full Text] [PDF]


Home page
J. Lipid Res.Home page
C. Xie, L. A. Woollett, S. D. Turley, and J. M. Dietschy
Fatty acids differentially regulate hepatic cholesteryl ester formation and incorporation into lipoproteins in the liver of the mouse
J. Lipid Res., September 1, 2002; 43(9): 1508 - 1519.
[Abstract] [Full Text] [PDF]


Home page
JAMAHome page
E. J. Schaefer, S. Lamon-Fava, J. L. Jenner, J. R. McNamara, J. M. Ordovas, C. E. Davis, J. M. Abolafia, K. Lippel, and R. I. Levy
Lipoprotein(a) Levels and Risk of Coronary Heart Disease in Men: The Lipid Research Clinics Coronary Primary Prevention Trial
JAMA, April 6, 1994; 271(13): 999 - 1003.
[Abstract] [PDF]


Home page
ANN INTERN MEDHome page
M. J. MALLOY, J. P. KANE, S. T. KUNITAKE, and P. TUN
Complementarity of Colestipol, Niacin, and Lovastatin in Treatment of Severe Familial Hypercholesterolemia
Ann Intern Med, November 1, 1987; 107(5): 616 - 623.
[Abstract] [PDF]