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Nutrition and Disease

Individual Trans Octadecenoic Acids and Partially Hydrogenated Vegetable Oil Differentially Affect Hepatic Lipid and Lipoprotein Metabolism in Golden Syrian Hamsters^1,2,3

⁴ Department of Animal Science, Cornell University, Ithaca, NY 14853 ⁵ Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853 ⁶ Division of Nutritional Biochemistry, School of Biosciences, University of Nottingham, Sutton Bonnington Campus, Loughborough, Leicestershire LE 12 5RD, UK ⁷ Department of Animal Science, University of Vermont, Burlington, VT 05405 ⁸ Nestle Research Center, Vers-chez-les-Blanc, CH-1000 Lausanne, Switzerland

Trans fatty acids (TFA) from industrial sources [i.e. partially hydrogenated vegetable oil (PHVO)] have been associated with several chronic human diseases, especially coronary heart disease (CHD). The possible contribution of individual TFA to overall CHD risk remains largely unknown. The objective of the present study was to investigate the effects of 2 major trans 18:1 isomers, trans-9 18:1 [elaidic acid (EA)] and trans-11 18:1 [vaccenic acid (VA)] on plasma lipid biomarkers of CHD risk. Thirty-two male Golden Syrian hamsters were randomly assigned to 1 of 4 dietary treatments: 1) control "Western" diet; 2) PHVO supplement; 3) EA supplement; and 4) VA supplement. Fat supplements were incorporated into the respective treatment diets at 2.5 g/100 g of diet. Compared with the control diet, the PHVO diet increased the plasma ratios of total:HDL-cholesterol and nonHDL:HDL-cholesterol by 17 and 23%, respectively. In contrast, these values decreased by 27 and 46% after the EA treatment and 8 and 14% after the VA treatment, respectively, indicating an improvement (reduction) in CHD risk. With regard to liver lipids, the EA diet reduced the content of (n-3) and (n-6) PUFA relative to the other treatments, suggesting an inhibition of enzymes common to the 2 biosynthesis pathways. Overall, results demonstrate that the hypercholesterolemic effects of PHVO are not dependent on the presence of EA or VA and that other bioactive components in PHVO must be responsible for its associated adverse health effects.

^* To whom correspondence should be addressed. E-mail: deb6{at}cornell.edu.

Manuscript received 11 August 2008. Initial review completed 22 September 2008. Revision accepted 5 November 2008.

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