Liu Jia, Li Changmeng, Yang Yun, Li Jingtao, Sun Xiaoguang, Zhang Yinqiang, Liu Runping, Chen Fafeng, Li Xiaojiaoyang
School of Life Sciences, Beijing University of Chinese Medicine, Beijing, 100029, China.
School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, 100029, China.
Cell Biosci. 2025 Apr 12;15(1):44. doi: 10.1186/s13578-025-01382-1.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic and systemic metabolic liver disease characterized by the presence of hepatic steatosis and at least one cardiometabolic risk factor (CMRF). The pathogenesis of MASLD involves multiple mechanisms, including lipid metabolism disorders, insulin resistance, inflammatory responses, and the hepato-intestinal axis of metabolic dysfunction. Among these factors, diet serves as both an inducement and a potential remedy in the disease's development. Notably, a high-lipid diet exacerbates fat accumulation, oxidative stress, and inflammatory responses, thereby promoting the progression of MASLD. Consequently, dietary induction models have become vital tools for studying the pathological mechanisms of MASLD, providing a foundation for identifying potential therapeutic targets. Additionally, we summarize the therapeutic effects of dietary optimization on MASLD and elucidate the role of specific dietary components in regulating the hepato-intestinal axis, lipid metabolism, and inhibiting inflammatory responses. In conclusion, studies utilizing animal models of MASLD offer significant insights into dietary therapy, particularly concerning the regulation of lipid metabolism-related and hepatoenteric axis-related signaling pathways as well as the beneficial mechanism of probiotics in hepatoenteric regulation. By understanding the specific mechanisms by which different dietary patterns affect MASLD, we can assess the clinical applicability of current dietary strategies and provide new directions for research and treatment aimed at disease modification.
代谢功能障碍相关脂肪性肝病(MASLD)是一种慢性全身性代谢性肝病,其特征为存在肝脂肪变性和至少一种心血管代谢危险因素(CMRF)。MASLD的发病机制涉及多种机制,包括脂质代谢紊乱、胰岛素抵抗、炎症反应以及代谢功能障碍的肝肠轴。在这些因素中,饮食在该疾病的发展过程中既是诱因又是潜在的治疗方法。值得注意的是,高脂饮食会加剧脂肪堆积、氧化应激和炎症反应,从而促进MASLD的进展。因此,饮食诱导模型已成为研究MASLD病理机制的重要工具,为确定潜在治疗靶点奠定了基础。此外,我们总结了饮食优化对MASLD的治疗效果,并阐明了特定饮食成分在调节肝肠轴、脂质代谢和抑制炎症反应中的作用。总之,利用MASLD动物模型进行的研究为饮食治疗提供了重要见解,特别是在调节脂质代谢相关和肝肠轴相关信号通路以及益生菌在肝肠调节中的有益机制方面。通过了解不同饮食模式影响MASLD的具体机制,我们可以评估当前饮食策略的临床适用性,并为旨在改善疾病的研究和治疗提供新方向。