Key result
Dietary linoleate shows ~6-fold greater plasma cholesteryl ester incorporation than oleate or palmitate.
Why the study?
The selectivity of lecithin:cholesterol acyltransferase and the relative contributions of LCAT and hepatic ACAT to the molecular composition of plasma cholesterol ester in humans and rats required evaluation.
LCAT selectivity for linoleate in human cholesteryl esters is supported; leaves open relevance to dietary fat metabolism or cardiovascular risk.
Selectivity factors (Vm/Km) for human and rat lecithin: cholesterol acyltransferases (LCAT) for the transfer of various acyl groups from the 2-position of phosphatidylcholine were determined. By multiplying these values by the proportions of acyl groups at the 2-position of phosphatidylcholine, one can predict the proportions of molecular species of cholesterol ester which will be synthesized by LCAT. In human subjects fasted overnight, the molecular composition of plasma cholesterol ester was found to reflect the LCAT selectivity relatively accurately. This result supports the concepts that hepatic acyl-CoA:cholesterol acyltransferase (ACAT) does not contribute significantly to the synthesis of plasma cholesterol ester and that removal of cholesterol ester from plasma is not selective with respect to molecular species under these conditions. In contrast to the results with humans, the molecular composition of plasma cholesterol ester formed in spontaneously hypertensive rats fed a high-cholesterol diet and then fasted overnight differs from that which is predicted from LCAT selectivity and the proportion of various fatty acids at the 2-position of phosphatidylcholine: these results suggest that cholesterol ester is formed mainly via the ACAT reaction.
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Ueno et al. (1986) studied Healthy individuals (postprandial fatty acid metabolism) (n=12). Test meal containing [U-13C]linoleate, [U-13C]oleate, and [U-13C]palmitate vs. Within-subject comparison among the three isotopically labeled fatty acids was evaluated on Postprandial metabolic partitioning and incorporation of [U-13C]linoleate, [U-13C]oleate, and [U-13C]palmitate into blood lipid fractions over 24 hours (p=<0.001). Dietary [U-13C]linoleate incorporation into plasma cholesteryl esters at 24 hours was over 6-fold greater than [U-13C]oleate and [U-13C]palmitate (P<0.001), while [U-13C]oleate predominated in VLDL-TG.
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