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Volume 205, Issue 1, Pages 197-201 (July 2009)


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Effects of intensive atorvastatin and rosuvastatin treatment on apolipoprotein B-48 and remnant lipoprotein cholesterol levels

Seiko Otokozawaab, Masumi Aiab, Thomas Van Himbergenb, Bela F. Asztalosab, Akira Tanakac, Evan A. Steind, Peter H. Jonese, Ernst J. SchaeferabCorresponding Author Informationemail address

Received 23 May 2008; received in revised form 30 October 2008; accepted 4 November 2008. published online 06 February 2009.

Abstract 

Atorvastatin and rosuvastatin at maximal doses are both highly effective in lowering low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG) levels. Rosuvastatin has been shown to be more effective than atorvastatin in lowering LDL-C, small dense LDL-C and in raising high-density lipoprotein (HDL) and its subclasses. Intestinal lipoproteins containing apolipoprotein (apo) B-48 are also thought to be atherogenic particles. Our purpose in this study was to compare the effects of daily oral doses of atorvastatin 80mg/day and rosuvastatin 40mg/day over a 6-week period on serum apo B-48 (a marker of intestinal lipoproteins) and remnant lipoprotein cholesterol (RemL-C) levels (a marker of partially metabolized lipoproteins of both intestinal and liver origin), using novel direct assays in 270 hyperlipidemic men and women. Both atorvastatin and rosuvastatin caused significant (p<0.0001) and similar median decreases in TG (−33.0%, −27.6%), RemL-C (−58.7%, −61.5%), and apoB-48 (−37.5%, −32.1%) as compared to baseline. Our findings utilizing a specific immunoassay and a fairly large number of subjects extend prior studies indicating that statins significantly lower apolipoprotein B containing lipoproteins of both intestinal and liver origin.

a Cardiovascular Research Laboratory, Friedman School of Nutrition Science and Policy at Tufts University and Tufts University School of Medicine, United States

b Lipid Metabolism Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, United States

c Nutrition Clinic, Kagawa Nutrition University, Tokyo, Japan

d Metabolic and Atherosclerosis Research Center, Cincinnati, OH, United States

e Baylor College of Medicine, Houston, TX, United States

Corresponding Author InformationCorresponding author at: Tufts University, 711 Washington Street, Boston, MA 02111, USA. Tel.: +1 617 556 3100; fax: +1 617 556 3103.

PII: S0021-9150(08)00778-8

doi:10.1016/j.atherosclerosis.2008.11.001


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