文献类型：期刊文献

英文题名：CD36 and DGAT2 facilitate the lipid-lowering effect of chitooligosaccharides via fatty acid intake and triglyceride synthesis signaling

作者：Shen, Xin[1];Liang, Xinyi[1];Ji, Xiaoguo[1];You, Jiangshan[1];Zhuang, Xinye[1];Song, Yudong[1];Yin, Hao[2];Zhao, Mengyao[1];Zhao, Liming[1,3]

机构：[1]East China Univ Sci & Technol, R&D Ctr Separat & Extract Technol Fermentat Ind, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]Shanghai Changzheng Hosp, Organ Transplant Ctr, Shanghai 200003, Peoples R China;[3]Shanghai Collaborat Innovat Ctr Biomfg Technol SC, Shanghai 200237, Peoples R China

年份：2021

卷号：12

期号：18

起止页码：8681

外文期刊名：FOOD & FUNCTION

收录：;EI(收录号：20213910943837);WOS:【SCI-EXPANDED(收录号:WOS:000681404200001)】；

基金：This work was financially supported by the National Key Research and Development Project (2019YFD0901805, 2017YFB0309302), China Postdoctoral Science Foundation (2019T120314), the National Natural Science Foundation for Young Scientists of China (No. 31801668), Shanghai PuJiang Program (18PJ1401900), the 111 Project (B18022) and Research Program of State Key Laboratory of Bioreactor Engineering (ZDXM2019).

语种：英文

外文关键词：Biosynthesis - Cholesterol - Proteins - Mammals

摘要：This study examined the impact of chitobiose (GlcN)(2) and chitotriose (GlcN)(3) on lipid accumulation modification and their inhibitory functionalities. (GlcN)(2) and (GlcN)(3) significantly inhibited the total cholesterol (TC), triglyceride (TG), and low-density lipid cholesterol (LDL-c) levels in the liver of the ob/ob(-/-) mice fed a non-high-fat diet. This phenomenon was associated with a reduction in the mRNA and protein expression of TG synthesis and fatty acid uptake-related signaling, significantly affecting the cluster of differentiation 36 (CD36) and diacylglycerol acyltransferase 2 (DGAT2). Furthermore, the CD36 and DGAT2 genes were overexpressed by constructing a plasmid and transfecting it into HepG2 cells, after which the phenotypic traits of lipid accumulation were assessed in vitro. Consequently, it was evident that (GlcN)(2) and (GlcN)(3) reduced the overexpression of these proteins and relieved cellular lipid accumulation. In conclusion, these results indicated that (GlcN)(2) and (GlcN)(3) acted positively against NAFLD while regulating steatosis in the non-high-fat diet NAFLD model. The potential NAFLD treatment strategies, such as targeting CD36 and DGAT2 signaling, could provide scientific insight into further applying food-derived ingredients to reduce the risk of high-fat metabolism.