Abstract

Introduction: Dietary oxidized lipids have been suggested to contribute to atherosclerosis. We have previously shown that oxidized linoleic acid (OxLA) modulates plasma lipids, feeding C57BL mice oxidized linoleic acid resulted in decreased plasma triglycerides and increased HDL. The current study is designed to investigate the mechanisms involved in the regulation of plasma lipids by the OxLA. Experimental Design: C57BL6 male mice (N=40) were divided into four groups (n = 10 each): Animals were fed for two months three different formulated diet except for the plain control (P) which was kept on normal mouse. The other three groups were as follows: control group supplemented with 18 mg/animal/day of linoleic acid (LA) (C); experimental group feed low concentration (9 mg/animal/day) of OxLA (A), and experimental group fed high dose of OxLA (18 mg/animal/day). After two months of feeding mice were sacrificed, blood, liver, and adipose tissues were collected for the analysis of plasma lipids, and related analyts and gene expressions for genes associated with lipoproteins metabolism. Results and Conclusion: The plasma total cholesterol and LDL have significantly (P<0.007) decreased in the high concentration OxLA compared to the group fed LA; this was accompanied with decreases in the high concentration OxLA plasma TG although is not significant. There were no observed significant differences in the plasma lipids between the plain control and the OxLA high dose, and between the controls on LA and the low concentration OxLA. We have observed a significant dose dependent decreases in plasma ApoC3 in mice fed low OxLA (P<0.01) and high OxLA (P<0.003) compared to the control group on LA. Plasma lipase levels have shown similar trends; decreasing significantly (P<0.04) in the OxLA groups compared to the plain controls. Plasma ApoA5 levels on the other hand greatly increased in high OxLA, LA, and low OxLA compared to plain group although is not significant. This study demonstrate that oxidized linoleic acid modulate plasma lipoprotein metabolism in mice through a likely ApoC3/lipase dependent mechanism(s).

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