title: Contribution of postprandial lipemia to the dietary fat-mediated changes in endogenous lipoprotein-cholesterol concentrations in humans.
abstract: 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.
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Atherosclerosis Research Unit, Medical School, University of Alabama at Birmingham, and the Moore Heart Research Foundation, University of Illinois, Champaign, IL, USA. bhchung@uab.edu
authors.forename: Byung-Hong
authors.initials: BH
authors.lastname: Chung
authors.forename: B H Simon
authors.initials: BH
authors.lastname: Cho
authors.forename: Ping
authors.initials: P
authors.lastname: Liang
authors.forename: Steve
authors.initials: S
authors.lastname: Doran
authors.forename: Laura
authors.initials: L
authors.lastname: Osterlund
authors.forename: Robert A
authors.initials: RA
authors.lastname: Oster
authors.forename: Betty
authors.initials: B
authors.lastname: Darnell
authors.forename: Frank
authors.initials: F
authors.lastname: Franklin
mesh_terms: D000328:Adult; D002784:Cholesterol / Q000097:blood*; D018592:Cross-Over Studies; D004041:Dietary Fats / Q000494:pharmacology*; D005215:Fasting / Q000097:blood; D005227:Fatty Acids / Q000008:administration & dosage / Q000494:pharmacology*; D005231:Fatty Acids, Unsaturated / Q000008:administration & dosage / Q000494:pharmacology*; D005260:Female; D006801:Humans; D008055:Lipids / Q000097:blood*; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D019518:Postprandial Period; D014280:Triglycerides / Q000097:blood
chemical_list: D004041:Dietary Fats; D005227:Fatty Acids; D005231:Fatty Acids, Unsaturated; D008055:Lipids; D008074:Lipoproteins; D014280:Triglycerides; C030104:lipoprotein cholesterol; D002784:Cholesterol