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<p>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.</p> Graphical Abstract <p>The double-edged sword role of dietary intake in the development of MASLD. An unhealthy diet leads to hepatic steatosis, fat accumulation, oxidative stress, and inflammation. In contrast, a balanced diet can prevent or alleviate MASLD progression.</p>

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Special correlation between diet and MASLD: positive or negative?

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年4月12日

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  • Jia Liu,
  • Changmeng Li,
  • Yun Yang,
  • Jingtao Li,
  • Xiaoguang Sun,
  • Yinqiang Zhang,
  • Runping Liu,
  • Fafeng Chen,
  • Xiaojiaoyang Li

摘要

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.

Graphical Abstract

The double-edged sword role of dietary intake in the development of MASLD. An unhealthy diet leads to hepatic steatosis, fat accumulation, oxidative stress, and inflammation. In contrast, a balanced diet can prevent or alleviate MASLD progression.