title: Alcohol-mediated enhancement of postprandial lipemia: a contributing factor to an increase in plasma HDL and a decrease in risk of cardiovascular disease.
abstract: BACKGROUND
  Moderate alcohol consumption increases plasma HDL and lowers cardiovascular disease risk while transiently enhancing postprandial lipemia.
  
  
  OBJECTIVE
  We hypothesized that the alcohol-mediated increase in postprandial triacylglycerol-rich lipoproteins (TRLs) and their clearance elevate HDL cholesterol and reverse cholesterol transport.
  
  
  METHODS
  We determined the effect in normolipidemic humans (n = 14) of postprandial lipemia produced 4 h after a test meal (M) or a test meal + 0.5 g alcohol/kg body wt (M+A) on postprandial changes in plasma lipids and on the balance of cholesterol between TRL and the cholesterol-rich LDL and HDL fractions (CRL) or red blood cells (RBCs) in fresh and incubated plasma or blood.
  
  
  RESULTS
  Postprandial lipemia after the M and M+A test meals caused a 56% and 89% increase in plasma triacylglycerol, a 30% and 74% increase in TRL cholesterol, and a 3.8% and 6.6% decrease in CRL cholesterol, respectively. In vitro reaction of endogenous lecithin:cholesterol acyltransferase (EC 2.3.1.43) and cholesteryl ester transfer proteins via incubation of fasting plasma samples and postprandial M and M+A plasma samples for 16 h increased TRL cholesterol by 22.8% (0.08 mmol/L), 32.6% (0.16 mmol/L), and 45.8% (0.28 mmol/L) in plasma and by 71.1% (0.27 mmol/L), 89.4% (0.45 mmol/L), and 112.5% (0.70 mmol/L) in RBC-enriched blood, respectively. After the in vitro lipolysis of TRL, the elevation of HDL cholesterol in postprandial M+A plasma, but not in postprandial M plasma, was significantly greater than in fasting plasma.
  
  
  CONCLUSIONS
  The alcohol-mediated increase in postprandial TRL flux and the hepatic removal of postprandial TRL after the acceptance of cholesterol from CRL and cell membranes contribute to increased HDL cholesterol and enhancement of reverse cholesterol transport in humans.
authors.affiliation: Department of Medicine, School of Medicine, University of Alabama, Birmingham, 35294, USA. bhchung@uab.edu
authors.forename: Byung-Hong
authors.initials: BH
authors.lastname: Chung
authors.forename: Steve
authors.initials: S
authors.lastname: Doran
authors.forename: Ping
authors.initials: P
authors.lastname: Liang
authors.forename: Laura
authors.initials: L
authors.lastname: Osterlund
authors.forename: B H Simon
authors.initials: BH
authors.lastname: Cho
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; D000428:Alcohol Drinking; D001692:Biological Transport; D002318:Cardiovascular Diseases / Q000517:prevention & control*; D002352:Carrier Proteins / Q000502:physiology; D002784:Cholesterol / Q000378:metabolism; D053480:Cholesterol Ester Transfer Proteins; D008076:Cholesterol, HDL / Q000097:blood*; D004910:Erythrocyte Membrane / Q000378:metabolism; D005260:Female; D006023:Glycoproteins; D006801:Humans; D008074:Lipoproteins / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000502:physiology; D019518:Postprandial Period / Q000502:physiology*; D012306:Risk; D014280:Triglycerides / Q000378:metabolism
chemical_list: C506642:CETP protein, human; D002352:Carrier Proteins; D053480:Cholesterol Ester Transfer Proteins; D008076:Cholesterol, HDL; D006023:Glycoproteins; D008074:Lipoproteins; D014280:Triglycerides; D002784:Cholesterol; D007862:Phosphatidylcholine-Sterol O-Acyltransferase