Wan Mei, Zhao Weimin, Cai Yifan, He Qian, Zeng Jun
The First Clinical Medical College of China Three Gorges University, Department of Endocrinology, Institute of Endocrine and Metabolic Diseases, Yichang Central People's Hospital Yichang 443000, Hubei, China.
Yichang Key Laboratory of Endocrinology Yichang 443000, Hubei, China.
Am J Transl Res. 2025 May 15;17(5):3276-3292. doi: 10.62347/ZWSR4476. eCollection 2025.
Non-alcoholic fatty liver disease (NAFLD) has emerged as a global health challenge due to its rising prevalence and strong association with metabolic syndrome. Recent studies highlight the critical role of the gut-brain axis (GBA)-a bidirectional communication system between the gut, brain, and liver-in NAFLD pathogenesis. Dysregulation of this axis can worsen metabolic dysfunction, inflammation, and liver injury. This review discusses the mechanisms driving GBA dysregulation in NAFLD, including alterations in gut microbiota, increased intestinal permeability, neuroinflammation, and imbalances in the autonomic nervous system (ANS). We also explore therapeutic strategies, such as microbiota modulation, vagus nerve stimulation, and neuroprotective interventions, that may help mitigate the effects of GBA dysfunction on NAFLD progression.
非酒精性脂肪性肝病（NAFLD）因其患病率不断上升以及与代谢综合征的密切关联，已成为一项全球性的健康挑战。近期研究突显了肠-脑轴（GBA）——肠道、大脑和肝脏之间的双向通信系统——在NAFLD发病机制中的关键作用。该轴的失调会加剧代谢功能障碍、炎症和肝损伤。本综述讨论了NAFLD中驱动GBA失调的机制，包括肠道微生物群的改变、肠道通透性增加、神经炎症以及自主神经系统（ANS）失衡。我们还探讨了治疗策略，如微生物群调节、迷走神经刺激和神经保护干预措施，这些策略可能有助于减轻GBA功能障碍对NAFLD进展的影响。
