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Sargassum fusiforme polysaccharide attenuates high-sugar–induced lipid accumulation in HepG2 cells and Drosophila melanogaster larvae
Food Science & Nutrition ( IF 3.5 ) Pub Date : 2021-08-12 , DOI: 10.1002/fsn3.2521 Dan He 1, 2 , Liping Yan 1 , Jiaqi Zhang 1 , Fang Li 1 , Yu Wu 1 , Laijin Su 1 , Peichao Chen 1 , Mingjiang Wu 1 , Jong-Il Choi 2 , Haibin Tong 1
Food Science & Nutrition ( IF 3.5 ) Pub Date : 2021-08-12 , DOI: 10.1002/fsn3.2521 Dan He 1, 2 , Liping Yan 1 , Jiaqi Zhang 1 , Fang Li 1 , Yu Wu 1 , Laijin Su 1 , Peichao Chen 1 , Mingjiang Wu 1 , Jong-Il Choi 2 , Haibin Tong 1
Affiliation
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.
中文翻译:
马尾藻梭形多糖减轻高糖诱导的 HepG2 细胞和果蝇幼虫中的脂质积累
脂质积累是非酒精性脂肪肝(NAFLD)发展的主要因素。目前,缺乏针对NAFLD的干预或治疗药物。在本研究中,我们研究了羊栖菜多糖 (SFPS) 减少 HepG2 细胞和果蝇幼虫中高糖诱导的脂质积累的能力。结果表明,SFPS 显着 ( p < .01) 减少了高糖诱导的 HepG2 细胞中脂滴的积累。此外,SFPS 还抑制这些细胞中Srebp和Fas (参与脂肪生成的基因)的表达,并增加PPARɑ和Cpt1 (参与脂肪酸 β-氧化的基因)的表达。 SFPS 显着降低了由高蔗糖饮食饲养的黑腹果蝇卵发育的第三龄幼虫的甘油三酯含量。幼虫中Srebp和Fas基因的表达也受到抑制,而参与脂肪酸 β-氧化的两个基因Acox57D-d和Fabp 在幼虫脂肪体(人类脂肪体的功能同源物)中表达增加。肝脏)。我们还发现 SFPS 可以改善高蔗糖饮食引起的发育异常。本研究的这些结果表明,SFPS 有可能用作预防和治疗 NAFLD 的治疗剂。
更新日期:2021-10-08
中文翻译:
马尾藻梭形多糖减轻高糖诱导的 HepG2 细胞和果蝇幼虫中的脂质积累
脂质积累是非酒精性脂肪肝(NAFLD)发展的主要因素。目前,缺乏针对NAFLD的干预或治疗药物。在本研究中,我们研究了羊栖菜多糖 (SFPS) 减少 HepG2 细胞和果蝇幼虫中高糖诱导的脂质积累的能力。结果表明,SFPS 显着 ( p < .01) 减少了高糖诱导的 HepG2 细胞中脂滴的积累。此外,SFPS 还抑制这些细胞中Srebp和Fas (参与脂肪生成的基因)的表达,并增加PPARɑ和Cpt1 (参与脂肪酸 β-氧化的基因)的表达。 SFPS 显着降低了由高蔗糖饮食饲养的黑腹果蝇卵发育的第三龄幼虫的甘油三酯含量。幼虫中Srebp和Fas基因的表达也受到抑制,而参与脂肪酸 β-氧化的两个基因Acox57D-d和Fabp 在幼虫脂肪体(人类脂肪体的功能同源物)中表达增加。肝脏)。我们还发现 SFPS 可以改善高蔗糖饮食引起的发育异常。本研究的这些结果表明,SFPS 有可能用作预防和治疗 NAFLD 的治疗剂。