首页> 美国卫生研究院文献>Marine Drugs >Chitosan Oligosaccharides Improve Glucolipid Metabolism Disorder in Liver by Suppression of Obesity-Related Inflammation and Restoration of Peroxisome Proliferator-Activated Receptor Gamma (PPARγ)
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Chitosan Oligosaccharides Improve Glucolipid Metabolism Disorder in Liver by Suppression of Obesity-Related Inflammation and Restoration of Peroxisome Proliferator-Activated Receptor Gamma (PPARγ)

机译:壳聚糖寡糖通过抑制肥胖相关的炎症和过氧化物酶体增殖物激活的受体γ(PPARγ)的恢复来改善肝脏的糖脂代谢紊乱。

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摘要

Chitosan oligosaccharides (COS) display various biological activities. In this study, we aimed to explore the preventive effects of COS on glucolipid metabolism disorder using palmitic acid (PA)-induced HepG2 cells and high-fat diet (HFD)-fed C57BL/6J mice as experimental models in vitro and in vivo, respectively. The results showed that COS pretreatment for 12 h significantly ameliorated lipid accumulation in HepG2 cells exposed to PA for 24 h, accompanied by a reversing of the upregulated mRNA expression of proinflammatory cytokines (IL-6, MCP-1, TNF-α) and glucolipid metabolism-related regulators (SCD-1, ACC1, PCK1-α). In addition, COS treatment alleviated glucolipid metabolism disorder in mice fed with HFD for five months, including reduction in body weight and fasting glucose, restoration of intraperitoneal glucose tolerance, and suppression of overexpression of proinflammatory cytokines and glucolipid metabolism-related regulators. Furthermore, our study found that COS pretreatment significantly reversed the downregulation of PPARγ at transcriptional and translational levels in both PA-induced HepG2 cells and liver tissues of HFD-fed mice. In summary, the study suggests that COS can improve glucolipid metabolism disorder by suppressing inflammation and upregulating PPARγ expression. This indicates a novel application of COS in preventing and treating glucolipid metabolism-related diseases.
机译:壳聚糖低聚糖(COS)具有多种生物活性。在这项研究中,我们旨在探索以棕榈酸(PA)诱导的HepG2细胞和高脂饮食(HFD)喂养的C57BL / 6J小鼠为实验模型的COS对糖脂代谢异常的预防作用,作为体内和体外实验模型,分别。结果表明,COS预处理12 h可以显着改善暴露于PA 24 h的HepG2细胞中的脂质蓄积,同时可以逆转促炎性细胞因子(IL-6,MCP-1,TNF-α)和糖脂的mRNA表达上调。代谢相关调节剂(SCD-1,ACC1,PCK1-α)。此外,COS治疗可减轻喂食HFD五个月的小鼠的糖脂代谢紊乱,包括减轻体重和禁食葡萄糖,恢复腹膜内葡萄糖耐量,抑制促炎性细胞因子和与糖脂代谢相关的调节剂的过表达。此外,我们的研究发现,COS预处理在PA诱导的HFD G2细胞和HFD喂养的小鼠肝组织中,均在转录和翻译水平上显着逆转了PPARγ的下调。总之,该研究表明COS可通过抑制炎症和上调PPARγ表达来改善糖脂代谢紊乱。这表明COS在预防和治疗糖脂代谢相关疾病中的新应用。

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