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Exogenous Oxidation of Lipids Reduces The Deleterious Effects of A High Fat Diet Composed of These Lipids in A Swine Model of Familial Hypercholesterolemia and Spontaneous Atherosclerosis
Author(s) -
Arowolo Folagbayi,
Meudt Jennifer J.,
Cabelka Colin,
Schomberg Dominic T.,
Chesmore Nathan J.,
López Ana Cecilia Escobar,
Trace Sam T.,
Reichert Jamie L.,
Crenshaw Thomas D.,
Richards Mark P.,
Shanmuganayagam Dhanansayan
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.684.19
Subject(s) - context (archaeology) , calorie , dyslipidemia , chemistry , food science , cholesterol , micronutrient , endocrinology , medicine , biology , biochemistry , disease , paleontology , organic chemistry
High‐fat diets elevate the risk of atherosclerotic cardiovascular disease (CVD), especially in individuals susceptible to dyslipidemia. Dietary fats consumed in westernized countries contain increasingly higher proportions of lipid oxidation byproducts, such as lipid hydroperoxides (LPOs), because of changes in agricultural, food processing, and cooking practices over the years. Although the formation of LPOs within the body is recognized as a central driver of the atherosclerotic process, it is unclear what impact exogenous (dietary) LPOs have in this context. We postulated that LPOs in the diet would not pose the same risk because of existing mechanisms for mitigating their absorption at the gastrointestinal level. Thus, we examined whether the conversion of a portion of lipids into LPOs by deep frying would reduce the atherogenicity of a high‐fat diet composed of such lipids in a novel swine model of spontaneous atherosclerosis. We placed four‐month old swine with familial hypercholesterolemia on the following isocaloric dietary regimens for four months: (1) [Control, N=6] low‐fat swine diet (~9% calories from fat); (2) [HF–LPOs, N=5] high‐fat diet (~44% calories from fat) containing negligible amounts of LPOs; (3) [HF+LPOs, N=5] high‐fat diet (~44% calories from fat) containing LPOs generated by heating of oil under an established protocol. The diets delivered equal amounts of micronutrients. Body weight (BW) measurements and serum samples were obtained at baseline and monthly during the study. At the end of the study period, the animals were euthanized and tissue harvested for gross and histological analysis of atherogenesis. Compared to the Control group, the HF–LPOs group showed a 58.5±20.4% increase in total serum cholesterol (TSC), while the HF+LPOs group only showed a 38.5±9.1% increase in TSC. Compared to HF–LPOs group, HF+LPOs showed a 20±11% lower BW gain over the course of the study; there was no notable difference in food intake. Compared to the Control group, the HF–LPOs group showed a 45.6±44.2% higher degree of atherogenesis in the aorta, while the HF+LPOs group only showed a 21.5±38.5% higher atherogenesis. The findings, taken together, suggest that oxidation of a portion of fats in the diet reduces the deleterious effects of the fat by potentially reducing the amount that is absorbed. Support or Funding Information The research was supported by the Biomedical & Genomic Research Group Discretionary Fund, University of Wisconsin‐Madison.