Alcohol Consumption Raises HDL Cholesterol Levels by Increasing the Transport Rate of Apolipoproteins A-I and A-II

Author:

De Oliveira e Silva Elizabeth R.1,Foster David1,McGee Harper Monnie1,Seidman Cynthia E.1,Smith Jonathan D.1,Breslow Jan L.1,Brinton Eliot A.1

Affiliation:

1. 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.

Abstract

Background —Moderate 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 Results —We 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 (Pearson’s 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). Conclusions —Alcohol 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.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

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