脂肪生成
CD36
化学
油酸
甘油三酯
脂肪酸
生物化学
脂质代谢
过氧化物酶体增殖物激活受体
脂肪变性
过氧化物酶体
内科学
内分泌学
受体
生物
胆固醇
医学
作者
Xiaodan Li,Mengyao Zhao,Liqiang Fan,Xuni Cao,Liehuan Chen,Junhui Chen,Yuan‐Hao Lo,Liming Zhao
标识
DOI:10.1016/j.jff.2018.04.058
摘要
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.
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