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Free access | 10.1172/JCI106896

Metabolic relationships among the plasma lipoproteins: Reciprocal changes in the concentrations of very low and low density lipoproteins in man

Dana E. Wilson and Robert S. Lees

1Clinical Research Center and the Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142

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

1Clinical Research Center and the Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142

Find articles by Lees, R. in: PubMed | Google Scholar

Published May 1, 1972 - More info

Published in Volume 51, Issue 5 on May 1, 1972
J Clin Invest. 1972;51(5):1051–1057. https://doi.org/10.1172/JCI106896.
© 1972 The American Society for Clinical Investigation
Published May 1, 1972 - Version history
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Abstract

The changes in other plasma lipoproteins which accompany alterations in very low density lipoproteins (VLDL) were studied in 31 normal and hyperlipidemic men and women who underwent weight reduction, carbohydrate induction, or clofibrate treatment. Plasma lipids and individual lipoprotein cholesterol concentrations were measured serially during control and treatment periods. Low density lipoprotein (LDL) protein was determined by radial immunodiffusion. Oppositely directed changes in VLDL and LDL were found with each of the three metabolic perturbations. Changes in high density lipoprotein (HDL) cholesterol generally paralleled those in LDL but were less consistent. Two patients with type III hyperlipoproteinemia failed to demonstrate reciprocal increases in LDL despite more than 40% reduction in plasma glycerides or VLDL with weight reduction or clofibrate therapy. After clofibrate therapy, LDL increased in proportion to the absolute decrease in VLDL cholesterol during treatment. LDL protein changed relatively less than did LDL cholesterol. The mechanism for the interdependency of plasma VLDL and LDL concentrations over the long term is not known and may be the result of altered rates of interconversion of these lipoproteins, or to feedback inhibition by VLDL of LDL production and release.

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