Published online before print April 15, 2004, doi: 10.1161/01.ATV.0000128410.23161.be
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© 2004 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
Dietary Hydrogenated Fat Increases High-Density Lipoprotein apoA-I Catabolism and Decreases Low-Density Lipoprotein apoB-100 Catabolism in Hypercholesterolemic Women
From Cardiovascular Nutrition (N.R.M., C.H., A.H.L.), Mass Spectrometry (G.G.D.), and Lipid Metabolism Laboratories (E.J.S.), Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, Mass; Division of Cardiology (F.K.W.), Beth Israel Deaconess Medical Center, Boston Mass; School of Medicine and Pharmacology (P.H.R.B.), University of Western Australia and Western Australia Institute for Medical Research, Perth, Australia; Department of Pathology (J.S.P.), Section on Comparative Medicine, Wake Forest University School of Medicine, Winston-Salem, NC; and Department of Medicine, Division of Endocrinology, Metabolism, and Diabetes (R.H.E.), University of Colorado Health Sciences Center, Denver, Co.
Correspondence to Dr Nirupa Matthan, Cardiovascular Nutrition Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston MA 02111. E-mail nirupa.matthan{at}tufts.edu
Objective— To determine mechanisms contributing to decreased high-density lipoprotein cholesterol (HDL-C) and increased low-density lipoprotein cholesterol (LDL-C) concentrations associated with hydrogenated fat intake, kinetic studies of apoA-I, apoB-100, and apoB-48 were conducted using stable isotopes.
Methods and Results— Eight postmenopausal hypercholesterolemic women were provided in random order with 3 diets for 5-week periods. Two-thirds of the fat was soybean oil (unsaturated fat), stick margarine (hydrogenated fat), or butter (saturated fat). Total and LDL-C levels were highest after the saturated diet (P<0.05; saturated versus unsaturated) whereas HDL-C levels were lowest after the hydrogenated diet (P<0.05; hydrogenated versus saturated). Plasma apoA-I levels and pool size (PS) were lower, whereas apoA-I fractional catabolic rate (FCR) was higher after the hydrogenated relative to the saturated diet (P<0.05). LDL apoB-100 levels and PS were significantly higher, whereas LDL apoB-100 FCR was lower with the saturated and hydrogenated relative to the unsaturated diet. There was no significant difference among diets in apoA-I or B-100 production rates or apoB-48 kinetic parameters. HDL-C concentrations were negatively associated with apoA-I FCR (r=–0.56, P=0.03) and LDL-C concentrations were negatively correlated with LDL apoB-100 FCR (r=–0.48, P=0.05).
Conclusions— The mechanism for the adverse lipoprotein profile observed with hydrogenated fat intake is determined in part by increased apoA-I and decreased LDL apoB-100 catabolism.
Hydrogenated fat intake decreases HDL-C and increases LDL-C concentrations. To determine mechanism, apoprotein kinetic studies were conducted in 8 women after consumption of an unsaturated, hydrogenated, or saturated diet. Hydrogenated fat intake resulted in higher HDL–apoA-I and lower LDL–apoB-100 catabolism, which were negatively correlated with HDL-C and LDL-C concentrations, respectively.
Key Words: trans fatty acids • hydrogenated fat • apolipoprotein kinetics • stable isotopes • soybean oil • margarine • butter
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