Dietary phosphatidylcholine supplementation reduces atherosclerosis in Ldlr−/− male mice2 |
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| Institution: | 1. Food and Nutritional Science, Department of Agricultural, University of Alberta, Edmonton, Alberta, Canada;2. Department of Biochemistry, University of Alberta, Edmonton, Alberta, Canada;1. College of Food Science and Engineering/Collaborative Innovation Center for Modern Grain Circulation and Safety/Key Laboratory of Grains and Oils Quality Control and Processing, Nanjing University of Finance and Economics, Nanjing, China;2. Basic Medical College, Nanjing University of Chinese Medicine, Nanjing, China;1. Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, Yamagata, Japan;2. Department of Immunology, Faculty of Medicine, Yamagata University, Yamagata, Japan;3. Department of Pathological Diagnostics, Faculty of Medicine, Yamagata University, Yamagata, Japan;4. Physical Chemistry for Life Science Laboratory, Faculty of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan;5. AMED-CREST, Japan Agency for Medical Research and Development, Chiyoda-ku, Tokyo, Japan;6. Miyata Diabetes and Metabolism Clinic, Fukushima-ku, Osaka, Japan;1. Cardiovascular Nutrition Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging, Friedman School of Nutrition Science and Policy, Tufts University, Boston, Massachusetts, USA;2. USDA, ARS, Beltsville Human Nutrition Research Center, Diet Genomics and Immunology Laboratory, Beltsville, Maryland, USA;3. Laboratory of Mucosal Barrier Pathobiology, Department of Pathology, Brigham and Woman''s Hospital and Harvard Medical School, Boston, Massachusetts, USA;4. Section of Preventive Medicine and Epidemiology, Boston University School of Medicine, Boston, Massachusetts, USA;5. Intercollege Graduate Degree Program in Physiology and Department of Nutritional Science, Pennsylvania State University, University Park, Pennsylvania, USA;1. Department of Pharmacy, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan;2. School of Pharmacy, Kaohsiung Medical University, Kaohsiung, Taiwan;3. Department of Seafood Science, National Kaohsiung University of Science and Technology, Kaohsiung, Taiwan;4. Center for Environmental Toxin and Emerging-Contaminant Research, Cheng Shiu University, Kaohsiung, Taiwan;5. Super Micro Mass Research and Technology Center, Cheng Shiu University, Kaohsiung, Taiwan;6. Institute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan;7. Division of Nephrology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan;8. Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan;1. United States Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center, Grand Forks, North Dakota;2. School of Public Health and Health Sciences, University of Massachusetts, Amherst, Massachusetts;3. School of Food and Agriculture, University of Maine, Orono, Maine |
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| Abstract: | Choline is an essential nutrient required for various biological processes. Eggs, dairy, and meat are rich in phosphatidylcholine (PC), whereas cereal and legumes are rich in free choline. Excess dietary choline leads to increase plasma trimethylamine N-oxide (TMAO). Epidemiological studies suggest that plasma TMAO is a biomarker for atherosclerosis and it has been suggested that a lower intake of eggs and meat would reduce choline consumption and thus reduce atherosclerosis development. To investigate whether the form of dietary choline influences atherosclerosis development in Ldlr−/−, we randomly fed Ldlr−/−male mice (aged 8 – 10 wk) one of the three 40% (calories) high fat diets (with 0.5% w/w of cholesterol): Control (0.1% w/w free-choline, CON), choline-supplemented (0.4% free-choline, CS), or PC-supplemented (0.1% free-choline and 0.3% choline from PC, PCS). After 12-wk of dietary intervention, the animals were euthanized and tissues and blood collected. Aortic atherosclerotic plaque area, plasma choline, lipid metabolites, and spleen and peripheral blood cell phenotypes were quantified. Surprisingly, the PCS group had significantly lower atherosclerotic lesions while having 2-fold higher plasma TMAO levels compared with both CON and CS groups (P<0.05). In the fasting state, we found that PCS decreased plasma very low-density lipoprotein-cholesterol (VLDL-C) and apolipoprotein B48 (APOB48), and increased plasma high-density lipoprotein-cholesterol (HDL-C). However, very low-density lipoprotein (VLDL) secretion was not affected by dietary treatment. We observed lower levels of circulating pro-atherogenic chemokines in the PCS group. Our study suggests that increased dietary PC intake does not induce a pro-atherogenic phenotype. |
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