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Journal of Lipid Research, Vol. 44, 1192-1198, June 2003
Copyright © 2003 by Lipid Research, Inc.

Effect of atorvastatin on postprandial lipoprotein metabolism in hypertriglyceridemic patients

Klaus G. Parhofer^1,*, Ester Laubach^* and P. Hugh R. Barrett^,

^* Department of Internal Medicine II, Grosshadern, Ludwig-Maximilians University, Munich, Germany
Department of Medicine, University of Western Australia, Perth, Western Australia
The Western Australian Institute for Medical Research, Perth, Western Australia

¹ To whom correspondence should be addressed. e-mail: 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 (10 mg/day) on postprandial lipoprotein metabolism in 10 hypertriglyceridemic patients (age, 40 ± 3 years; body mass index, 27 ± 1 kg/m²; cholesterol, 5.74 ± 0.34 mmol/l; triglycerides, 3.90 ± 0.66 mmol/l; HDL-cholesterol, 0.85 ± 0.05 mmol/l; and LDL-cholesterol, 3.18 ± 0.23 mmol/l). Patients were randomized to be studied with or without atorvastatin therapy. Postprandial lipoprotein metabolism was evaluated with a standardized oral fat load. Plasma was obtained every 2 h for 14 h. Large triglyceride-rich lipoproteins (TRLs) (containing chylomicrons) and small TRLs (containing chylomicron remnants) were isolated by ultracentrifugation, and cholesterol, triglyceride, apolipoprotein B-100 (apoB-100), apoB-48, apoC-III, and retinyl-palmitate concentrations were determined. Atorvastatin significantly (P < 0.01) decreased fasting cholesterol (-27%), triglycerides (-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, -triglycerides, and -retinyl-palmitate, while none of the small TRL parameters changed. These findings contrast with the results in normolipidemic subjects, in which atorvastatin decreased the AUC for chylomicron remnants (small TRLs) but not for chylomicrons (large TRLs).

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.

Abbreviations: apo, apolipoprotein; AUC, area under the curve; BMI, body mass index; LPL, lipoprotein lipase; TRL, triglyceride-rich lipoprotein

Supplementary key words triglyceride-rich lipoprotein • chylomicrons • chylomicron remnants • retinyl palmitate

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