In this study, C57BL/6 mice were given an HFHSD diet for 8 weeks to induce hepatic steatosis and then given COSM solution orally for 12 weeks. The study found that the HFHSD diet resulted in steatosis and insulin resistance in mice. The formation of NAFLD induced by HFHSD diet was related to the imbalance of intestinal flora. However, after COSM intervention, the abundance of beneficial bacteria increased significantly, while the abundance of harmful bacteria decreased significantly. The HFHSD diet also induced changes in intestinal bacterial metabolites, and the content of short-chain fatty acids in cecal contents after COSM intervention was significantly higher than that in the model group. In addition, COSM not only improved LPS levels and barrier dysfunction in the ileum and colon but upregulated protein levels of ZO-1, occludin, and claudin in the colon and downregulated the liver LPS/TLR4/NF-κB inflammatory pathway. We concluded that the treatment of marine chitooligosaccharide COSM could improve the intestinal microflora structure of the fatty liver and activate an inflammatory signaling pathway, thus alleviating the intrahepatic lipid accumulation induced by HFHSD.

中文翻译：

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海洋壳寡糖改变肠道菌群结构并调节肝脏炎症反应以影响非酒精性脂肪肝

在这项研究中，C57BL/6 小鼠被给予 HFHSD 饮食 8 周以诱导肝脏脂肪变性，然后口服 COSM 溶液 12 周。研究发现，HFHSD 饮食导致小鼠出现脂肪变性和胰岛素抵抗。HFHSD饮食诱发NAFLD的形成与肠道菌群失衡有关。然而，经COSM干预后，有益菌丰度显着增加，而有害菌丰度显着下降。HFHSD饮食也引起肠道细菌代谢物的变化，COSM干预后盲肠内容物中短链脂肪酸含量显着高于模型组。此外，COSM 不仅改善了回肠和结肠的 LPS 水平和屏障功能障碍，而且上调了 ZO-1、occludin、和结肠中的密蛋白并下调肝脏 LPS/TLR4/NF-κB 炎症通路。我们得出结论，海洋壳寡糖 COSM 的治疗可以改善脂肪肝的肠道菌群结构并激活炎症信号通路，从而减轻 HFHSD 诱导的肝内脂质积累。