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Journal of Lipid Research, Vol 35, 1583-1591, Copyright © 1994 by Lipid Research, Inc.
ARTICLES |
RW James and D Pometta
Lipid Laboratory, University Hospital, Switzerland.
The behavior of apolipoprotein-defined subpopulations LpAI and LpAI,AII within high density lipoprotein (HDL) subclasses 2 and 3 was analyzed in the postprandial phase after a fat load. For the whole group of subjects, increases in plasma concentrations of HDL, principally due to the influx of lipoprotein surface components, were largely confined to the HDL3 density range and involved LpAI,AII and LpAI. However, the degree of postprandial lipemia influenced the distribution of surface remnants between the subfractions. In subjects with a limited postprandial rise in triglycerides, increased HDL mass was predominantly associated with LpAI,AII, and equally distributed between HDL2 and HDL3. Conversely, subjects with exaggerated postprandial lipemia manifested increased mass primarily within the HDL3 density range, implicating both LpAI,AII and LpAI. Stepwise regression analysis identified a two-variable model, involving LpAI,AII within HDL2 and LpAI within HDL3, as best defining the relationship between postprandial lipemia and the increase in HDL mass. Postprandial increases in triglyceride content were observed for all HDL subfractions, whilst modifications to the core lipid mass ratios were significant only for LpAI,AII. Stepwise regression analysis revealed a significant correlation between postprandial lipemia and the increase in triglyceride concentration only of LpAI,AII within HDL3. The results suggest that postprandial lipemia differentially influences apolipoprotein-defined HDL subfractions. The extent of postprandial lipemia may determine the involvement of different HDL subfractions in postprandial lipoprotein metabolism.
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