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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-CoA, implying that CP administration can promote hepatic fatty acid β-oxidation. The present results demonstrate the underlying mechanisms of CP in high-fat diet-induced NAFLD rats and suggest that CP treatment might provide a dietary therapeutic tool for the treatment of NAFLD in humans.


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Chicory polysaccharides alleviate high-fat diet-induced non-alcoholic fatty liver disease via alteration of lipid metabolism- and inflammation-related gene expression

Show Author's information Shengjie Lia,bYulong Wua,bHaitao Jianga,bFeng Zhoua,bAiling Bena,cRenlei WangdChun Huaa,b( )
School of Food Science, Nanjing Xiaozhuang University, Nanjing 211171, China
Jiangsu Provincial Key Construction Laboratory of Special Biomass Byproduct Resource Utilization, Nanjing 211171, China
Nanjing Key Laboratory of Quality and safety of agricultural products, Nanjing 211171, China
Biology Department, Jiangsu Second Normal University, Nanjing 210013, China

Peer review under responsibility of KeAi Communications Co., Ltd.

Abstract

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-CoA, implying that CP administration can promote hepatic fatty acid β-oxidation. The present results demonstrate the underlying mechanisms of CP in high-fat diet-induced NAFLD rats and suggest that CP treatment might provide a dietary therapeutic tool for the treatment of NAFLD in humans.

Keywords: Transcriptome, Metabolome, Chicory polysaccharides, Non-alcoholic fatty liver disease

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Received: 27 September 2020
Revised: 26 November 2020
Accepted: 01 December 2020
Published: 28 April 2022
Issue date: July 2022

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© 2022 Beijing Academy of Food Sciences. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co., Ltd.

Acknowledgements

Acknowledgements

This work was 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 (SUJIAOYANHAN[2022]No.2), Excellent Scientific and Technological Innovation Team of Colleges and Universities of Jiangsu Province (SUJIAOKE[2021]No.1), the Key Subject of Biology of Nanjing (NINGJIAOGAOSHI[2021]No.16) and the Youth program of Nanjing Xiaozhuang University (2019NXY47). We would like to thank Editage (www.editage.cn) for English language editing.

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This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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