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)

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.