4.7 Article

Dietary phosphatidylcholine supplementation reduces atherosclerosis in Ldlr-/- male mice2

Journal

JOURNAL OF NUTRITIONAL BIOCHEMISTRY
Volume 92, Issue -, Pages -

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jnutbio.2021.108617

Keywords

Phosphatidylcholine. choline; trimethylamine N-oxide; atherosclerosis; Ldlr(-/-) mice

Funding

  1. Natural Sciences and Engineering Research Council [RES 0025104]
  2. Quality Food for Health grant from the Alberta Livestock and Meat Agency
  3. Mexican National Council for Science and Technology Scholarship

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Choline is an essential nutrient that plays a role in various biological processes, and the form of dietary choline intake can influence the development of atherosclerosis. Increased intake of phosphatidylcholine in the diet may reduce the risk of atherosclerosis but is associated with higher plasma TMAO levels.
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. (C) 2021 Elsevier Inc. All rights reserved.

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