Dietary Flaxseed Oil Prevents Western-Type Diet-Induced Nonalcoholic Fatty Liver Disease in Apolipoprotein-E Knockout Mice

• Published in: Oxidative medicine and cellular longevity Vol. 2017; no. 2017; pp. 1 - 13
• Main Authors: Li, Xiuhua, Tang, Haiying, Zhao, Haifeng, Qiu, Fubin, Han, Hao, Shi, Dongxing
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2017; Hindawi; John Wiley & Sons, Inc
• Subjects: Animals; Apolipoproteins; Apolipoproteins E - metabolism; Care and treatment; Cholesterol; Cytokines; Development and progression; Diet; Fatty acids; Fatty liver; Fish oils; Flaxseed oil; Food; Gastroenterology; Genetic aspects; Health aspects; Hepatology; Laboratory animals; Linseed Oil - chemistry; Lipids; Liver diseases; Male; Mice; Non-alcoholic Fatty Liver Disease - pathology; Non-alcoholic Fatty Liver Disease - prevention & control; Nutrition research; Oils & fats; Polyunsaturated fatty acids; Rodents; China
• ISSN: 1942-0900; 1942-0994; 1942-0994
• DOI: 10.1155/2017/3256241

The prevalence of nonalcoholic fatty liver disease (NAFLD) has dramatically increased globally during recent decades. Intake of n-3 polyunsaturated fatty acids (PUFAs), mainly eicosapentaenoic acid (EPA, C20:5n-3) and docosahexaenoic acid (DHA, C22:6n-3), is believed to be beneficial to the development of NAFLD. However, little information is available with regard to the effect of flaxseed oil rich in α-linolenic acid (ALA, C18:3n-3), a plant-derived n-3 PUFA, in improving NAFLD. This study was to gain the effect of flaxseed oil on NAFLD and further investigate the underlying mechanisms. Apolipoprotein-E knockout (apoE-KO) mice were given a normal chow diet, a western-type high-fat and high-cholesterol diet (WTD), or a WTD diet containing 10% flaxseed oil (WTD + FO) for 12 weeks. Our data showed that consumption of flaxseed oil significantly improved WTD-induced NAFLD, as well as ameliorated impaired lipid homeostasis, attenuated oxidative stress, and inhibited inflammation. These data were associated with the modification effects on expression levels of genes involved in de novo fat synthesis (SREBP-1c, ACC), triacylglycerol catabolism (PPARα, CPT1A, and ACOX1), inflammation (NF-κB, IL-6, TNF-α, and MCP-1), and oxidative stress (ROS, MDA, GSH, and SOD).