期刊
NUTRIENTS
卷 14, 期 12, 页码 -出版社
MDPI
DOI: 10.3390/nu14122530
关键词
ferulic acid; NAFLD; energy expenditure; beta-oxidation; ketone body biosynthesis
资金
- Key R&D programof Shaanxi China [2020ZDLNY05-07, 2021NY-126]
- National Key RD Program [2021YFD1000305]
Ferulic acid (FA) has a protective effect on high-fat diet-induced non-alcoholic fatty liver disease (NAFLD) by activating PPARα to decrease triacylglycerol accumulation and increase energy expenditure.
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据