Ferulic Acid Prevents Nonalcoholic Fatty Liver Disease by Promoting Fatty Acid Oxidation and Energy Expenditure in C57BL/6 Mice Fed a High-Fat Diet
文献类型： 外文期刊
作者： Luo, Zhixin 1 ; Li, Mengqian 1 ; Yang, Qiong 1 ; Zhang, Yuhong 2 ; Liu, Fang 1 ; Gong, Lan 3 ; Han, Lin 1 ; Wang, Min 1 ;
作者机构： 1.Northwest A&F Univ, Coll Food Sci & Engn, Yangling 712100, Xianyang, Peoples R China
2.Tibet Acad Agr & Anim Husb Sci, Inst Food Sci & Technol, Lhasa 850000, Peoples R China
3.Univ New South Wales, St George & Sutherland Clin Sch, Microbiome Res Ctr, Sydney, NSW 2052, Australia
关键词： ferulic acid; NAFLD; energy expenditure; beta-oxidation; ketone body biosynthesis
期刊名称：NUTRIENTS （ 影响因子：6.706； 五年影响因子：7.185 ）
ISSN：
年卷期： 2022 年 14 卷 12 期
页码：
收录情况： SCI
摘要： There is a consensus that ferulic acid (FA), the most prominent phenolic acid in whole grains, displays a protective effect in non-alcoholic fatty liver disease (NAFLD), though its underlying mechanism not fully elucidated. This study aimed to investigate the protective effect of FA on high-fat diet (HFD)-induced NAFLD in mice and its potential mechanism. C57BL/6 mice were divided into the control diet (CON) group, the HFD group, and the treatment (HFD+FA) group, fed with an HFD and FA (100 mg/kg/day) by oral gavage for 12 weeks. Hematoxylin and eosin (H&E) staining and Oil Red O staining were used to evaluate liver tissue pathological changes and lipid accumulation respectively. It was demonstrated that FA supplementation prevented HFD-induced NAFLD, which was evidenced by the decreased accumulation of lipid and hepatic steatosis in the HFD+FA group. Specifically, FA supplementation decreased hepatic triacylglycerol (TG) content by 33.5% (p < 0.01). Metabolic cage studies reveal that FA-treated mice have elevated energy expenditure by 11.5% during dark phases. Mechanistically, FA treatment increases the expression of rate-limiting enzymes of fatty acid oxidation and ketone body biosynthesis CPT1A, ACOX1 and HMGCS2, which are the peroxisome proliferator-activated receptors alpha (PPAR alpha) targets in liver. In conclusion, FA could effectively prevent HFD-induced NAFLD possibly by activating PPAR alpha to increase energy expenditure and decrease the accumulation of triacylglycerol in the liver.
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