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Papers In Press, published online ahead of print February 21, 2007
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Department of Nutrition, Harvard School of Public Health, Boston, MA 02115
Corresponding Author: fsacks{at}hsph.harvard.edu
The atherogenicity theory for triglyceride-rich lipoproteins (TRL; VLDL+IDL) generally cites the action of apoCIII, a component of some TRL, to retard their metabolism in plasma. We studied kinetics of multiple TRL and LDL subfractions according to content of apoCIII and apoE, in eleven hypertriglyceridemic and normolipidemic persons. The liver secretes mainly two types of apoB lipoproteins: TRL with apoCIII and LDL without apoCIII. About 45% of TRL with apoCIII are secreted together with apoE. Contrary to expectation, TRL with apoCIII but not apoE have fast catabolism, losing some or all their apoCIII and becoming LDL. In contrast, apoE directs TRL flux toward rapid clearance, limiting LDL formation. TRL without apoCIII or apoE are a minor, slow metabolizing precursor of LDL with little direct removal. Elevated VLDL apoCIII levels are correlated with increased VLDL production rather than slow particle turnover. Finally, hypertriglyceridemics have significantly greater production of apoCIII containing VLDL and global prolongation in residence time of all particle types. ApoE may be the key determinant of the metabolic fate of atherogenic apoCIII containing TRL in plasma, channeling them toward removal from the circulation, and reducing the formation of LDL, both those with apoCIII and the main type without apoCIII.
Revised on January 31, 2007
Accepted on February 21, 2007
Rapid turnover of apolipoprotein CIII containing triglyceride-rich lipoproteins contributing to formation of LDL subfractions
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