Chicory polysaccharides alleviate high-fat diet-induced non-alcoholic fatty liver disease via alteration of lipid metabolism-and inflammation-related gene expression
Chicory polysaccharides alleviate high-fat diet-induced non-alcoholic fatty liver disease via alteration of lipid metabolism-and inflammation-related gene expression作者机构:School of Food ScienceNanjing Xiaozhuang UniversityNanjing 211171China Jiangsu Provincial Key Construction Laboratory of Special Biomass Byproduct Resource UtilizationNanjing 211171China Nanjing Key Laboratory of Quality and safety of agricultural productsNanjing 211171China Biology DepartmentJiangsu Second Normal UniversityNanjing 210013China
出 版 物:《Food Science and Human Wellness》 (食品科学与人类健康(英文))
年 卷 期:2022年第11卷第4期
页 面:954-964页
核心收录:
学科分类:0832[工学-食品科学与工程(可授工学、农学学位)] 08[工学] 083201[工学-食品科学]
基 金:supported by the Natural Science Foundation of the Jiangsu Higher Education Institutions of China (18KJD180002 20KJA416003 20KJA416003 18KJA180007) the Key Subject of Ecology of Jiangsu Province (SUJIAOYANHANNo.2) Excellent Scientific and Technological Innovation Team of Colleges and Universities of Jiangsu Province (SUJIAOKENo.1) the Key Subject of Biology of Nanjing (NINGJIAOGAOSHI No.16) the Youth program of Nanjing Xiaozhuang University (2019NXY47)
主 题:Chicory polysaccharides Non-alcoholic fatty liver disease Transcriptome Metabolome
摘 要:Administration of chicory polysaccharides(CP) can modify lipid metabolism, improve dyslipidemia, and reduce liver inflammation, all of which may help alleviate non-alcoholic fatty liver disease(NAFLD). However, the underlying mechanisms remain unclear. This study aimed to gain further understanding of the potential molecular mechanisms that mediate the protective effects of CP against NAFLD via transcriptomic and metabolomic analyses. Hepatic RNA-sequencing analysis demonstrated that long-term intake of CP restored expression of lipid metabolism-related genes Xbp1, Insig2, and Cth in NAFLD rats, thereby inhibiting de novo lipogenesis. Moreover, CP consumption restored expression levels of genes involved in pro-inflammatory responses, such as Irf1. In addition, metabolic data confirmed that CP treatment increased levels of L-palmitoylcarnitine and hexadecanoyl-Co A, implying that CP administration can promote hepatic fatty acid β-oxidation. The present results demonstrate the underlying mechanisms of CP in high-fat dietinduced NAFLD rats and suggest that CP treatment might provide a dietary therapeutic tool for the treatment of NAFLD in humans.