Fish Oil Significantly Alters Fatty Acid Profiles in Various Lipid Fractions but Not Atherogenesis in Apo E-KO Mice

Overview

Journal Eur J Nutr

Specialty Nutritional Sciences

Date 2007 Jan 18

PMID 17225919

Citations 8

Authors

Zuyuan Xu

Natalie Riediger

Sheila Innis

Mohammed H Moghadasian

Affiliations

Soon will be listed here.

Abstract

Background: Consumption of fish oil and n-3 fatty acids is associated with beneficial modifications in plasma lipid levels. The impact of these modifications on development of atherosclerotic lesions merits further investigation.

Aim Of The Study: The aim of this study was to investigate the impact of fish oil consumption on quality and quantity of lipoprotein fatty acids and its influence on atherosclerosis in apolipoprotein E-knockout (apo E-KO) mice.

Methods: Male apo E-KO mice were treated with 1% dietary fish oil for 14 weeks. Plasma triglycerides (TG), phospholipids, (PL) and cholesteryl ester (CE) fractions were separated using thin layer chromatography. Plasma-free fatty acids (FFA) plus fatty acid contents of TG, PL, CE were determined using gas chromatography. Aortic atherosclerosis was assessed by histological and morphometrical techniques.

Results: Twenty-eight fatty acids were identified in each of the four lipid compartments. High amounts of n-3 fatty acids (eicosapentaenoic (EPA), docosahexaenoic (DHA)) were found in all of these fractions. The levels of EPA and DHA increased by 400 and 150%, respectively, in FFA, TG and PL compartments; higher increases (>500 and 200%) in EPA and DHA were found in CE. This markedly decreased the n-6/n-3 ratios in FFA, TG, PL, and CE by 60, 72, 53, and 61%, respectively. These changes were accompanied by a significant increase in plasma triglyceride levels. Surprisingly, these changes did not affect atherogenesis.

Conclusions: Elevated levels of EPA and DHA do not appear to prevent development of atherosclerotic plaques in this model. Longer studies warrant investigation of the direct benefits of these fatty acids against myocardial damage as clinical consequences of advanced atherosclerosis.

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