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.

本研究探讨粗壳寡糖（COS）和五个特定的Coss（（葡萄糖胺）的改善效果_2-6）对脂质积聚和，其中，表征壳二糖的抑制机制（（葡萄糖胺）₂）。用油酸（OA）处理后，HepG2细胞中的甘油三酸酯（TG），LDL-c含量，脂肪生成信号基因和蛋白质增加，而COS和五个单COS在联合处理和后续处理中均抑制了脂质积聚。治疗。此外，我们观察到4 mg / mL（GlcN）₂对肝脂质蓄积具有显着抑制作用，并降低了二酰基甘油酰基转移酶2（DGAT2），肝X受体α（LXRα），过氧化物酶体增殖物激活受体-γ（PPARγ），孕烯醇酮X受体（PXR）和mRNA和蛋白表达分化簇36（CD36）。这些结果共同表明，在所有研究的（GlcN）_2-6中，（GlcN）₂通过减少HepG2细胞中的脂肪酸摄取和TG合成，为抗高脂血症和脂肪变性的调节提供了最佳的活性。