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Sargassum fusiforme polysaccharide attenuates high‐sugar–induced lipid accumulation in HepG2 cells and Drosophila melanogaster larvae
Lipid accumulation is a major factor in the development of non‐alcoholic fatty liver disease (NAFLD). Currently, there is a lack of intervention or therapeutic drugs against NAFLD. In this study, we investigated the ability of Sargassum fusiforme polysaccharide (SFPS) to reduce lipid accumulation in...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8498055/ https://www.ncbi.nlm.nih.gov/pubmed/34646529 http://dx.doi.org/10.1002/fsn3.2521 |
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author | He, Dan Yan, Liping Zhang, Jiaqi Li, Fang Wu, Yu Su, Laijin Chen, Peichao Wu, Mingjiang Choi, Jong‐il Tong, Haibin |
author_facet | He, Dan Yan, Liping Zhang, Jiaqi Li, Fang Wu, Yu Su, Laijin Chen, Peichao Wu, Mingjiang Choi, Jong‐il Tong, Haibin |
author_sort | He, Dan |
collection | PubMed |
description | Lipid accumulation is a major factor in the development of non‐alcoholic fatty liver disease (NAFLD). Currently, there is a lack of intervention or therapeutic drugs against NAFLD. In this study, we investigated the ability of Sargassum fusiforme polysaccharide (SFPS) to reduce lipid accumulation induced by high sugar in HepG2 cells and Drosophila melanogaster larvae. The results indicated that SFPS significantly (p < .01) decreased the accumulation of lipid droplets in high sugar–induced HepG2 cells. Furthermore, SFPS also suppressed the expression of Srebp and Fas (genes involved in lipogenesis) and increased the expression of PPARɑ and Cpt1 (genes that participated in fatty acid β‐oxidation) in these cells. SFPS markedly reduced the content of triglyceride of the third instar larvae developed from D. melanogaster eggs reared on the high‐sucrose diet. The expression of the Srebp and Fas genes in the larvae was also inhibited whereas the expression of two genes involved in the β‐oxidation of fatty acids, Acox57D‐d and Fabp, was increased in the larval fat body (a functional homolog of the human liver). We also found that SFPS ameliorated developmental abnormalities induced by the high‐sucrose diet. These results of this study suggest that SFPS could potentially be used as a therapeutic agent for the prevention and treatment of NAFLD. |
format | Online Article Text |
id | pubmed-8498055 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-84980552021-10-12 Sargassum fusiforme polysaccharide attenuates high‐sugar–induced lipid accumulation in HepG2 cells and Drosophila melanogaster larvae He, Dan Yan, Liping Zhang, Jiaqi Li, Fang Wu, Yu Su, Laijin Chen, Peichao Wu, Mingjiang Choi, Jong‐il Tong, Haibin Food Sci Nutr Original Research Lipid accumulation is a major factor in the development of non‐alcoholic fatty liver disease (NAFLD). Currently, there is a lack of intervention or therapeutic drugs against NAFLD. In this study, we investigated the ability of Sargassum fusiforme polysaccharide (SFPS) to reduce lipid accumulation induced by high sugar in HepG2 cells and Drosophila melanogaster larvae. The results indicated that SFPS significantly (p < .01) decreased the accumulation of lipid droplets in high sugar–induced HepG2 cells. Furthermore, SFPS also suppressed the expression of Srebp and Fas (genes involved in lipogenesis) and increased the expression of PPARɑ and Cpt1 (genes that participated in fatty acid β‐oxidation) in these cells. SFPS markedly reduced the content of triglyceride of the third instar larvae developed from D. melanogaster eggs reared on the high‐sucrose diet. The expression of the Srebp and Fas genes in the larvae was also inhibited whereas the expression of two genes involved in the β‐oxidation of fatty acids, Acox57D‐d and Fabp, was increased in the larval fat body (a functional homolog of the human liver). We also found that SFPS ameliorated developmental abnormalities induced by the high‐sucrose diet. These results of this study suggest that SFPS could potentially be used as a therapeutic agent for the prevention and treatment of NAFLD. John Wiley and Sons Inc. 2021-08-12 /pmc/articles/PMC8498055/ /pubmed/34646529 http://dx.doi.org/10.1002/fsn3.2521 Text en © 2021 The Authors. Food Science & Nutrition published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research He, Dan Yan, Liping Zhang, Jiaqi Li, Fang Wu, Yu Su, Laijin Chen, Peichao Wu, Mingjiang Choi, Jong‐il Tong, Haibin Sargassum fusiforme polysaccharide attenuates high‐sugar–induced lipid accumulation in HepG2 cells and Drosophila melanogaster larvae |
title |
Sargassum fusiforme polysaccharide attenuates high‐sugar–induced lipid accumulation in HepG2 cells and Drosophila melanogaster larvae |
title_full |
Sargassum fusiforme polysaccharide attenuates high‐sugar–induced lipid accumulation in HepG2 cells and Drosophila melanogaster larvae |
title_fullStr |
Sargassum fusiforme polysaccharide attenuates high‐sugar–induced lipid accumulation in HepG2 cells and Drosophila melanogaster larvae |
title_full_unstemmed |
Sargassum fusiforme polysaccharide attenuates high‐sugar–induced lipid accumulation in HepG2 cells and Drosophila melanogaster larvae |
title_short |
Sargassum fusiforme polysaccharide attenuates high‐sugar–induced lipid accumulation in HepG2 cells and Drosophila melanogaster larvae |
title_sort | sargassum fusiforme polysaccharide attenuates high‐sugar–induced lipid accumulation in hepg2 cells and drosophila melanogaster larvae |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8498055/ https://www.ncbi.nlm.nih.gov/pubmed/34646529 http://dx.doi.org/10.1002/fsn3.2521 |
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