He Dan, Yan Liping, Zhang Jiaqi, Li Fang, Wu Yu, Su Laijin, Chen Peichao, Wu Mingjiang, Choi Jong-Il, Tong Haibin
College of Life and Environmental Science Wenzhou University Wenzhou China.
Department of Biotechnology and Bioengineering Chonnam National University Gwangju South Korea.
Food Sci Nutr. 2021 Aug 12;9(10):5590-5599. doi: 10.1002/fsn3.2521. eCollection 2021 Oct.
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 polysaccharide (SFPS) to reduce lipid accumulation induced by high sugar in HepG2 cells and larvae. The results indicated that SFPS significantly ( < .01) decreased the accumulation of lipid droplets in high sugar-induced HepG2 cells. Furthermore, SFPS also suppressed the expression of and (genes involved in lipogenesis) and increased the expression of and (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 eggs reared on the high-sucrose diet. The expression of the and genes in the larvae was also inhibited whereas the expression of two genes involved in the β-oxidation of fatty acids, and 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.
脂质蓄积是非酒精性脂肪性肝病（NAFLD）发展的主要因素。目前，针对NAFLD缺乏干预措施或治疗药物。在本研究中，我们研究了多糖（SFPS）减少高糖诱导的HepG2细胞和幼虫中脂质蓄积的能力。结果表明，SFPS显著（<0.01）减少了高糖诱导的HepG2细胞中脂滴的蓄积。此外，SFPS还抑制了这些细胞中参与脂肪生成的基因和的表达，并增加了参与脂肪酸β氧化的基因和的表达。SFPS显著降低了由高糖饮食饲养的卵发育而来的三龄幼虫的甘油三酯含量。幼虫中基因和的表达也受到抑制，而参与脂肪酸β氧化的两个基因和在幼虫脂肪体（人类肝脏的功能同源物）中的表达增加。我们还发现SFPS改善了高糖饮食诱导的发育异常。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。
