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(Circulation. 2000;102:2347.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
From The Rockefeller University (E.R. De O. e S., C.E.S., J.D.S., J.L.B.), New York, NY; University of Washington (D.F.) (Seattle); Hunter College (M.M.H.), City University of New York; and Carl T. Hayden VA Medical Center (E.A.B.), Phoenix, Ariz.
Correspondence to Jan L. Breslow, Laboratory of Biochemical Genetics and Metabolism, Box 179, The Rockefeller University, 1230 York Ave, New York, NY 10021-6399. E-mail breslow{at}rockvax.rockefeller.edu
BackgroundModerate alcohol intake is associated with lower atherosclerosis risk, presumably due to increased HDL cholesterol (HDL-C) concentrations; however, the metabolic mechanisms of this increase are poorly understood.
Methods and ResultsWe tested the hypothesis that ethanol increases HDL-C by raising transport rates (TRs) of the major HDL apolipoproteins apoA-I and -II. We measured the turnover of these apolipoproteins in vivo in paired studies with and without alcohol consumption in 14 subjects. The fractional catabolic rate (FCR) and TR of radiolabeled apoA-I and -II were determined in the last 2 weeks of a 4-week Western-type metabolic diet, without (control) or with alcohol in isocaloric exchange for carbohydrates. Alcohol was given as vodka in fixed amounts ranging from 0.20 to 0.81 g · kg-1 · d-1 (mean±SD 0.45±0.19) to reflect the usual daily intake of each subject. HDL-C concentrations increased 18% with alcohol compared with the control (Wilcoxon matched-pairs test, P=0.002). The apoA-I concentrations increased by 10% (P=0.048) and apoA-II concentrations increased by 17% (P=0.005) due to higher apoA-I and -II TRs, respectively, whereas the FCR of both apoA-I and -II did not change. The amount of alcohol consumed correlated with the degree of increase in HDL-C (Pearsons r=0.66, P=0.01) and apoA-I TR (r=0.57, P=0.03). The increase in HDL-C also correlated with the increase in apoA-I TR (r=0.61, P=0.02).
ConclusionsAlcohol intake increases HDL-C in a dose-dependent fashion, associated with and possibly caused by an increase in the TR of HDL apolipoproteins apoA-I and -II.
Key Words: alcohol lipoproteins cholesterol apolipoproteins metabolism
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