Chitobiose alleviates oleic acid-induced lipid accumulation by decreasing fatty acid uptake and triglyceride synthesis in HepG2 cells

Abstract

This study investigates the ameliorative effect of crude chitooligosaccharide (COS) and five specific COSs ((GlcN)2-6) on lipid accumulation and, therein, characterizes the inhibition mechanism of chitobiose ((GlcN)2). After treatment with oleic acid (OA), the triglyceride (TG), LDL-c content, lipogenesis-signaling genes and protein in HepG2 cells increased, while lipid accumulation was suppressed by COS and five single COSs both in co-treatment and after-treatment. In addition, we observed that 4 mg/mL (GlcN)2 had a significant inhibitory effect on hepatic lipid accumulation and decreased the mRNA and protein expressions of diacylglycerol acyltransferase 2 (DGAT2), liver X receptor α (LXRα), peroxisome proliferator-activated receptor-γ (PPARγ), pregnenolone X receptor (PXR) and cluster of differentiation 36 (CD36). These results collectively indicate that, among all (GlcN)2-6 studied, (GlcN)2 provides the best active effect on anti-hyperlipidemia and steatosis regulation via decreasing fatty acid uptake and TG synthesis in HepG2 cells.

Keywords

• Chitobiose
• Hepatic steatosis
• Oleic acid
• CD36
• DGAT2