Dietary hydrogenated fat increases high-density lipoprotein apoA-I catabolism and decreases low-density lipoprotein apoB-100 catabolism in hypercholesterolemic women
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. Eigh...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology Jg. 24; H. 6; S. 1092 |
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01.06.2004
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| Abstract | 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.
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).
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. |
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| AbstractList | 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.
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).
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. 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.OBJECTIVETo 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.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).METHODS AND RESULTSEight 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).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.CONCLUSIONSThe 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. |
| Author | Barrett, P Hugh R Schaefer, Ernst J Dolnikowski, Gregory G Parks, John S Welty, Francine K Harausz, Carrie Lichtenstein, Alice H Matthan, Nirupa R Eckel, Robert H |
| Author_xml | – sequence: 1 givenname: Nirupa R surname: Matthan fullname: Matthan, Nirupa R email: nirupa.matthan@tufts.edu organization: Cardiovascular Nutrition Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston Mass 02111, USA. nirupa.matthan@tufts.edu – sequence: 2 givenname: Francine K surname: Welty fullname: Welty, Francine K – sequence: 3 givenname: P Hugh R surname: Barrett fullname: Barrett, P Hugh R – sequence: 4 givenname: Carrie surname: Harausz fullname: Harausz, Carrie – sequence: 5 givenname: Gregory G surname: Dolnikowski fullname: Dolnikowski, Gregory G – sequence: 6 givenname: John S surname: Parks fullname: Parks, John S – sequence: 7 givenname: Robert H surname: Eckel fullname: Eckel, Robert H – sequence: 8 givenname: Ernst J surname: Schaefer fullname: Schaefer, Ernst J – sequence: 9 givenname: Alice H surname: Lichtenstein fullname: Lichtenstein, Alice H |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/15087307$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Apolipoprotein A-I - blood Apolipoprotein B-100 Apolipoproteins B - blood Butter Cholesterol, HDL - blood Cholesterol, LDL - blood Cross-Over Studies Dietary Fats - pharmacology Double-Blind Method Female Humans Hypercholesterolemia - blood Kinetics Margarine Middle Aged Postmenopause Soybean Oil - pharmacology Trans Fatty Acids - pharmacology Triglycerides - blood |
| Title | Dietary hydrogenated fat increases high-density lipoprotein apoA-I catabolism and decreases low-density lipoprotein apoB-100 catabolism in hypercholesterolemic women |
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