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A more recent version of this article appeared on June 1, 2003

Papers In Press, published online ahead of print April 1, 2003
J. Lipid Res., doi:10.1194/jlr.M300011-JLR200
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Submitted on January 10, 2003
Revised on March 25, 2003
Accepted on March 25, 2003

Effect of atorvastatin on postprandial lipoprotein metabolism in hypertriglyceridemic patients

Klaus G. Parhofer, Ester Laubach, and P. Hugh R. Barrett

Medical Dept. II, Grosshadern, Munich 81377

Corresponding Author: parhofer{at}med2.med.uni-muenchen.de

Postprandial lipoprotein metabolism is impaired in hypertriglyceridemia. It is unknown how and to what extent atorvastatin affects postprandial lipoprotein metabolism in hypertriglyceridemic patients. We evaluated the effect of 4 weeks of atorvastatin therapy (10mg/day) on postprandial lipoprotein metabolism in 10 hypertriglyceridemic patients (age 40±3years, BMI 27±1kg/m2, cholesterol 5.74±0.34, triglyceride 3.90±0.66, HDL-cholesterol 0.85±0.05, LDL-cholesterol 3.18±0.23mmol/L). Patients were randomized to be studied either first with or without atorvastatin therapy. Postprandial lipoprotein metabolism was evaluated with a standardized oral fat load. Plasma was obtained every 2h for 14h. Large triglyceride-rich lipoproteins (TRL) (containing chylomicrons) and small TRL (containing chylomicron-remnants) were isolated by ultracentrifugation and cholesterol, triglyceride, apoB-100, apoB-48, apoC-III and retinyl-palmitate concentrations were determined. Atorvastatin significantly (p<0.01) decreased fasting cholesterol (-27%), triglyceride (-43%), LDL-cholesterol (-28%), and apoB-100 (-31%) and increased HDL-cholesterol (+19%). Incremental area under the curve (AUC) significantly (p<0.05) decreased for large TRL-cholesterol, -triglyceride, and -retinyl-palmitate, while none of the small TRL parameters changed. These findings contrast with the results in normolipidemic subjects where atorvastatin decreased AUC for chylomicron remnants (small TRL) but not for chylomicrons (large TRL). We conclude that atorvastatin improves postprandial lipoprotein metabolism in addition to decreasing fasting lipid levels in hypertriglyceridemia. Such changes would be expected to improve the atherogenic profile.


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