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Dietary Oxidized Linoleic Acid Modulates Plasma Lipids beyond Triglycerides Metabolism

INTRODUCTION: Triglyceride (TG) is an independent risk factor for coronary heart disease. Previous work has shown that short-term supplementations of mouse chow with oxidized linoleic acid (OxLA) significantly reduce the level of plasma triglycerides. STUDY OBJECTIVE: This study aims to determine th...

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Detalles Bibliográficos
Autores principales: Garelnabi, Mahdi, Ainsworth, Gregory, Mahini, Halleh, Jamil, Naseeha, Ochin, Chinedu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5727721/
https://www.ncbi.nlm.nih.gov/pubmed/29318046
http://dx.doi.org/10.1155/2017/1645828
Descripción
Sumario:INTRODUCTION: Triglyceride (TG) is an independent risk factor for coronary heart disease. Previous work has shown that short-term supplementations of mouse chow with oxidized linoleic acid (OxLA) significantly reduce the level of plasma triglycerides. STUDY OBJECTIVE: This study aims to determine the effects of longer-term supplementation of mouse chow with various concentrations of oxidized linoleic acid (OxLA) on plasma triglycerides. STUDY DESIGN: The study consisted of forty C57BL/6 wildtype mice divided into four groups (n = 10). Two groups were kept as controls. One control group (P) was fed plain chow and the second control group (C) was fed chow supplemented with linoleic acid. The other two experimental groups (A) and (B) were fed oxidized linoleic acid supplemented chow in the following doses: 9 mg/day of oxidized linoleic acid and 18 mg/day of oxidized linoleic acid/mouse. RESULTS AND CONCLUSION: Mice that were on a diet supplemented with the higher dose of oxidized linoleic acid showed a 39% decrease in hepatic PPAR-α and a significant decrease in the plasma HDL levels compared to the mice that were fed diets of plain and linoleic acid supplemented chow. Interestingly, the longer-term consumption of oxidized linoleic acid may predispose to atheropathogenesis.