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American Journal of Clinical Nutrition, Vol. 80, No. 5, 1145-1158, November 2004
© 2004 American Society for Clinical Nutrition


ORIGINAL RESEARCH COMMUNICATION

Contribution of postprandial lipemia to the dietary fat-mediated changes in endogenous lipoprotein-cholesterol concentrations in humans1,2,3

Byung-Hong Chung, BH Simon Cho, Ping Liang, Steve Doran, Laura Osterlund, Robert A Oster, Betty Darnell and Frank Franklin

1 From the Atherosclerosis Research Unit (B-HC, PL, SD, and LO), the General Clinical Research Center (RAS and BD), and the Departments of Medicine (B-HC, PL, SD, and LO), Pediatrics (FF), and Nutrition (FF), Medical School, University of Alabama at Birmingham, and the Moore Heart Research Foundation, University of Illinois, Champaign, IL (BHSC)

Background: Dietary fats alter LDL and HDL cholesterol while serving as precursors of postprandial triacylglycerol-rich lipoproteins (TRLs).

Objective: We hypothesized that the saturated fatty acid (SFA)–mediated increase and the polyunsaturated fatty acid (PUFA)–mediated decrease in endogenous lipoprotein cholesterol are promoted by postprandial TRLs.

Design: We performed a 16-d crossover diet study to examine the effect of PUFA-rich [ratio of PUFAs to SFAs (P:S) = 2.0] and SFA-rich (P:S = 0.25) diets on fasting and postprandial plasma lipid and lipoprotein-cholesterol concentrations in 16 normolipidemic subjects.

Results: Fasting plasma cholesterol decreased significantly after a PUFA-rich diet because of a decrease in LDL (–12.3%; P < 0.05) and HDL (–3.8%; NS), but did not change after an SFA-rich diet. The appearance of postprandial TRLs in plasma at 4 h was linked to a significant lowering of both LDL (–7.4%) and HDL (–4.8%) after a PUFA-rich diet; no such effect was observed after the SFA-rich diet. At 7 h, LDL and HDL cholesterol returned to near fasting concentrations without postprandial TRL accumulation after a PUFA-rich diet but with a significant postprandial TRL accumulation after an SFA-rich diet. Thus, the in vivo postprandial clearance of cholesterol in LDL+HDL was greater after a PUFA-rich diet than after an SFA-rich diet. The appearance of postprandial TRLs in plasma increased the cholesteryl ester transfer protein–mediated transfer of cholesteryl ester from LDL+HDL to TRLs in vitro without a significant influence from dietary fat.

Conclusion: Dietary fat–mediated alterations in the rate of hepatic removal of postprandial TRLs, which carry cholesterol accepted from LDL+HDL via cholesteryl ester transfer protein in vivo, may contribute to the dietary fat–mediated change in endogenous lipoprotein cholesterol.

Key Words: Chylomicrons • VLDL • LDL • HDL • lecithin:cholesterol acyltransferase • cholesteryl ester transfer proteins • postprandial lipemia • reverse cholesterol transport • polyunsaturated fat • saturated fat




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