文献类型：期刊文献

英文题名：Chitooligosaccharide supplementation prevents the development of high fat diet-induced non-alcoholic fatty liver disease (NAFLD) in mice via the inhibition of cluster of differentiation 36 (CD36)

作者：Zhao, Mengyao; Shen, Xin; Li, Xiaodan; Chen, Baoli; Fan, Liqiang; Xia, Quanming; Zhao, Liming

机构：[1]East China Univ Sci & Technol, Sch Biotechnol, State Key Lab Bioreactor Engn, R&D Ctr Separat & Extract Technol Fermentat Ind, Shanghai 200237, Peoples R China;[2]SCICBT, Shanghai 200237, Peoples R China

年份：2019

卷号：57

起止页码：7

外文期刊名：JOURNAL OF FUNCTIONAL FOODS

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000470053800002)】；

基金：This work was financially supported by the China Postdoctoral Science Foundation (2017M621392), the National Natural Science Foundation of China (31801668), the Shanghai PuJiang Program (18PJ1401900), and the Fundamental Research Funds for the Central Universities (222201814036). We also thank Dr. Runze Wu for his technical supporting on the modeling docking of CD36.

语种：英文

外文关键词：Chitooligosaccharide; Cluster of differentiation 36 (CD36); Non-alcoholic fatty liver disease (NAFLD); Free fatty acids uptake; Triglyceride synthesis

摘要：The effects of (GlcN)(2-3) on the development of high fat diet-induced non-alcoholic fatty liver disease in C57BL/6J mice and the potential structural-functional relationship between different singular degrees of polymerization (DPs) COSs and CD36 activity were investigated. (GlcN)(2-3) was found to significantly inhibit the levels of triglyceride, low density lipid protein and total cholesterol in the serum and liver, thus reducing hepatic steatosis and, ultimately, altering lipid accumulation. This phenomenon was associated with a decrease in the mRNA and protein expressions of CD36, PXR, DGAT2, LXR alpha and PPAR gamma, which subsequently decreased the uptake of FFAs and triglyceride synthesis. Using structural analysis, (GlcN)(2-3) blocked the core cavity and inhibited the trans location of FFAs in CD36. Furthermore, the molecular size and steric hindrance effect play crucial roles in the deactivation of CD36. These findings will provide a better understanding of the modulating actions of specific singular-DPs COS in high fat diet-induced hepatic steatosis.