ARTICLE
20 September 2026

睡眠剥夺与高果糖饮食诱导MAFLD 机制的研究进展及其协同作用

妍 陆1 ,  吉涛 宋1
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1 哈尔滨医科大学附属第二医院 消化内科, 中国
MRP 2026 , 4(9), 54–56; https://doi.org/10.61369/MRP.2026090029
© 2026 by the Author(s). Licensee Art and Technology, USA. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution -Noncommercial 4.0 International License (CC BY-NC 4.0) ( https://creativecommons.org/licenses/by-nc/4.0/ )
Abstract

代谢相关脂肪性肝病(MAFLD)已成为全球公共卫生的严峻挑战。现代生活方式中,睡眠稳态破坏与高果糖饮食伴随出现,二者存在潜在的非线性协同致病作用。本文系统综述了这两种环境应激在脂质从头合成、胰岛素信号传导及肠道微环境稳态中的交互作用机制,重点阐述“肠道氧化应激累积- 屏障功能崩溃- 菌群代谢物易位”这一轴线在连接环境压力与系统性炎症中的核心地位,并基于“生物钟- 代谢耦合”理论,探讨恢复昼夜节律与调整饮食习惯的联合干预策略。

Keywords
睡眠剥夺
高果糖饮食
MAFLD
肠道- 肝脏轴
胰岛素抵抗
氧化应激
References

[1]Byrne C D, Targher G. NAFLD: a multisystem disease[J]. Journal of Hepatology, 2015, 62(1 Suppl): S47-S64.
[2] Softic S, Cohen D E, Kahn C R. Role of dietary fructose and hepatic de novo lipogenesis in fatty liver disease[J]. Digestive Diseases and Sciences, 2016, 61(5): 1282-1293.
[3]Vaccaro A, Kaplan Dor Y, Nambara K, et al. Sleep loss can cause death through accumulation of reactive oxygen species in the gut[J]. Cell, 2020, 181(6): 1307-1328.e15.
[4]Tilg H, Adolph T E, Trauner M. Gut-liver axis: pathophysiological concepts and clinical implications[J]. Cell Metabolism, 2022, 34(11): 1700-1718.

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