Original Contributions |
From the Department of Animal Sciences (M.A.L.), Purdue University, West Lafayette, Ind; Divisions of Atherosclerosis, Nutrition and Lipid Research (B.W.P., R.T.K., G.S.), and Endocrinology, Diabetes and Metabolism (R.E.O.), Department of Medicine, Washington University; and Purina Mills, Inc (D.H.), St. Louis, Mo.
Correspondence to Dr Gustav Schonfeld, Department of Internal Medicine, Washington University School of Medicine, Box 8046, 660 S Euclid Ave, St. Louis, MO 63110. E-mail Gschonfeld{at}imgate.wustl.edu
AbstractAlcohol fed to rabbits in a liquid formula at 30% of calories increased plasma cholesterol by 36% in the absence of dietary cholesterol and by 40% in the presence of a 0.5% cholesterol diet. The increase was caused almost entirely by VLDL, IDL, and LDL. Cholesterol feeding decreased the fractional catabolic rate for VLDL and LDL apoprotein by 80% and 57%, respectively, and increased the production rate of VLDL and LDL apoprotein by 75% and 15%, respectively. Alcohol feeding had no effect on VLDL apoprotein production but increased LDL production rate by 55%. The efficiency of intestinal cholesterol absorption was increased by alcohol. In the presence of dietary cholesterol, percent cholesterol absorption rose from 34.4±2.6% to 44.9±2.5% and in the absence of dietary cholesterol, from 84.3±1.4% to 88.9±1.0%. Increased cholesterol absorption and increased LDL production rate may be important mechanisms for exacerbation by alcohol of hypercholesterolemia in the cholesterol-fed rabbit model.
Key Words: cholesterol alcohol diet cholesterol absorption lipoproteins apoproteins atherosclerosis
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