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Atherosclerosis. 2012 May;222(1):222-8. doi: 10.1016/j.atherosclerosis.2012.02.001. Epub 2012 Feb 7.

Postprandial accumulation of chylomicrons and chylomicron remnants is determined by the clearance capacity.

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Sahlgrenska Center for Cardiovascular and Metabolic Research/Wallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Sweden.



To better understand the postprandial clearance of triglyceride-rich lipoproteins (TRLs) and its relation to the fasting kinetics of TRLs.


Two studies were performed on 30 male subjects: a fasting kinetic study to determine the fasting secretion and clearance rates of apolipoprotein B (apoB) 100 and triglycerides in the very low-density lipoprotein 1 and 2 (VLDL(1) and VLDL(2)) fractions; and a postprandial study to determine the postprandial accumulation of apoB48, apoB100 and triglycerides in the chylomicron, VLDL(1) and VLDL(2) fractions. Results from these two studies were combined to characterize the postprandial clearance of TRLs in a physiologically relevant setting.


Our results show that postprandial accumulation of the apoB48-carrying chylomicrons can be predicted from the clearance capacity of the lipolytic pathway, determined in the fasting state. Furthermore, we show that chylomicrons and VLDL(1) particles are not cleared equally by the lipoprotein lipase pathway, and that chylomicrons seem to be the preferred substrate. Subjects with a rapid fasting lipid metabolism accumulate lower levels of postprandial triglycerides with less accumulation of apoB100 in the VLDL(1) fraction and a faster transfer of apoB100 into the VLDL(2) fraction. In contrast, fasting VLDL(1) secretion does not predict postprandial triglyceride accumulation.


Non-fasting triglyceride levels have recently been identified as a major predictor of future cardiovascular events. Here we show that the capacity of the lipolytic pathway is a common determinant of both the fasting and non-fasting triglyceride levels and may thus play an important role in the development of dyslipemia and atherosclerosis.

[Indexed for MEDLINE]

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