Alcohol-mediated enhancement of postprandial lipemia: a contributing factor to an increase in plasma HDL and a decrease in risk of cardiovascular disease.
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.
Chung
Byung-Hong
BH
Department of Medicine, School of Medicine, University of Alabama, Birmingham, 35294, USA. bhchung@uab.edu
Doran
Steve
S
Liang
Ping
P
Osterlund
Laura
L
Cho
B H Simon
BH
Oster
Robert A
RA
Darnell
Betty
B
Franklin
Frank
F
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
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