Postprandial hyperlipidemia and remnant lipoproteins

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Abstract
Improved methods for quantification of organ-specific contributions to postprandial hyperlipidemia indicate substantial increases in the concentration and altered properties of hepatogenous VLDL, in addition to accumulation of chylomicron remnants. Recent clinical studies support the hypothesis that small chylomicron remnants characterized by apolipoprotein (apo)B48 and VLDL remnants characterized by apolipoprotein B100 are atherogenic lipoproteins.