|Otokozawa, Seiko -|
|Ai, Masumi -|
|Van Himbergen, Thomas -|
|Asztalos, Bela -|
|Tanaka, Akira -|
|Stein, Evan -|
|Jones, Peter -|
|Schaefer, Ernst -|
Submitted to: Atherosclerosis
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: November 4, 2008
Publication Date: July 20, 2009
Citation: Otokozawa, S., Ai, M., Van Himbergen, T., Asztalos, B.F., Tanaka, A., Stein, E.A., Jones, P.H., Schaefer, E. 2009. Effects of intensive atorvastatin and rosuvastatin treatment on apolipoprotein B-48 and remnant lipoprotein cholesterol levels. Atherosclerosis. 205(1):197-201. Interpretive Summary: High cholesterol levels in blood can be reduced by treating a person with statins. Statins slow down the production of cholesterol and also lower one of the major cholesterol transport particles in the blood, the so-called apolipoprotein B (apoB). The two major producers of apoB in the human body are the liver and the intestine. The current study looked at two different statins (atorvastatin and rosuvastatin) and shows that people treated with these statins, lowered the apoB derived from both the liver as well as the intestine.
Technical 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 80 mg/day and rosuvastatin 40 mg/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.