State Key Laboratory of Food Science and Resources, Nanchang University, 235 Nanjing East Road, Nanchang 330047, China.
Jiangxi-OAI Joint Research Institute, Nanchang University, 235 Nanjing East Road, Nanchang 330047, China.
Nutrients. 2024 Mar 27;16(7):958. doi: 10.3390/nu16070958.
Non-alcoholic fatty liver disease (NAFLD) is a common chronic hepatic condition whose impact on human health is increasingly significant. The imbalance of the gut microbiome, linked to insulin resistance, heightened intestinal permeability, and pro-inflammatory reactions, may be the linchpin in the development of NAFLD. In our research, the impact of ZDY2013 administration for 12 weeks on gut microbiota dysbiosis induced by a high-fat, high-fructose, high-cholesterol (FHHC) diet in male C57BL/6n mice was investigated. Research results presented that the intervention of ZDY2013 in mice fed with the FHHC diet could restore their liver function and regulate oxidative stress. Compared to mice in the model group, the intervention of ZDY2013 significantly regulated the gut microbiota, inhibited the LPS/NF-κB pathway, and led to a lower level of colonic inflammation in the mice administered with ZDY2013. It also improved insulin resistance to regulate the PI3K/Akt pathway and lipid metabolism, thereby resulting in reduced fat accumulation in the liver. The above results suggest that the intervention of ZDY2013 can hinder the progression of diet-induced NAFLD by reducing inflammation to regulate the PI3K/Akt pathway and regulating gut microbiota disturbance.
非酒精性脂肪性肝病（NAFLD）是一种常见的慢性肝脏疾病，其对人类健康的影响日益显著。肠道微生物组的失衡与胰岛素抵抗、肠道通透性增加和促炎反应有关，可能是 NAFLD 发展的关键。在我们的研究中，研究了 ZDY2013 给药 12 周对高脂肪、高果糖、高胆固醇（FHHC）饮食诱导的雄性 C57BL/6n 小鼠肠道微生物失调的影响。研究结果表明，在 FHHC 饮食喂养的小鼠中，ZDY2013 的干预可以恢复其肝功能并调节氧化应激。与模型组小鼠相比，ZDY2013 的干预显著调节了肠道微生物群，抑制了 LPS/NF-κB 途径，导致接受 ZDY2013 治疗的小鼠结肠炎症水平降低。它还改善了胰岛素抵抗，调节了 PI3K/Akt 通路和脂质代谢，从而减少了肝脏中的脂肪堆积。上述结果表明，ZDY2013 的干预可以通过减少炎症来调节 PI3K/Akt 通路和调节肠道微生物群紊乱来阻止饮食诱导的 NAFLD 的进展。
