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Journal of Lipid Research, Vol. 48, 1746-1753, August 2007
Copyright © 2007 by American Society for Biochemistry and Molecular Biology

Effects of different doses of atorvastatin on human apolipoprotein B-100, B-48, and A-I metabolism

Stefania Lamon-Fava^1,*, Margaret R. Diffenderfer^*, P. Hugh R. Barrett, Aaron Buchsbaum^*, Nirupa R. Matthan, Alice H. Lichtenstein, Gregory G. Dolnikowski^**, Katalin Horvath^*, Bela F. Asztalos^*, Valeria Zago^* and Ernst J. Schaefer^*,

^* Lipid Metabolism Laboratory, Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA
Cardiovascular Nutrition Laboratory, Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA
^** Mass Spectrometry Laboratory, Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA
School of Medicine and Pharmacology, University of Western Australia, Perth, Australia
Cardiovascular Research Laboratory, Friedman School of Nutrition Science and Policy at Tufts University and Tufts University School of Medicine, Boston, MA

Published, JLR Papers in Press, May 27, 2007.

¹ To whom correspondence should be addressed. e-mail: stefania.lamon-fava{at}tufts.edu

Nine hypercholesterolemic and hypertriglyceridemic subjects were enrolled in a randomized, placebo-controlled, double-blind, crossover study to test the effect of atorvastatin 20 mg/day and 80 mg/day on the kinetics of apolipoprotein B-100 (apoB-100) in triglyceride-rich lipoprotein (TRL), intermediate density lipoprotein (IDL), and LDL, of apoB-48 in TRL, and of apoA-I in HDL. Compared with placebo, atorvastatin 20 mg/day was associated with significant reductions in TRL, IDL, and LDL apoB-100 pool size as a result of significant increases in fractional catabolic rate (FCR) without changes in production rate (PR). Compared with the 20 mg/day dose, atorvastatin 80 mg/day caused a further significant reduction in the LDL apoB-100 pool size as a result of a further increase in FCR. ApoB-48 pool size was reduced significantly by both atorvastatin doses, and this reduction was associated with nonsignificant increases in FCR. The lathosterol-campesterol ratio was decreased by atorvastatin treatment, and changes in this ratio were inversely correlated with changes in TRL apoB-100 and apoB-48 PR. No significant effect on apoA-I kinetics was observed at either dose of atorvastatin. Our data indicate that atorvastatin reduces apoB-100- and apoB-48-containing lipoproteins by increasing their catabolism and has a dose-dependent effect on LDL apoB-100 kinetics. Atorvastatin-mediated changes in cholesterol homeostasis may contribute to apoB PR regulation.

Supplementary key words kinetics • lathosterol • campesterol

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