<?xml version="1.1" encoding="utf-8"?>
<article xsi:noNamespaceSchemaLocation="http://jats.nlm.nih.gov/publishing/1.1/xsd/JATS-journalpublishing1-mathml3.xsd" dtd-version="1.1" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"><front><journal-meta><journal-id journal-id-type="publisher-id">MRP</journal-id><journal-title-group><journal-title>Medical Research and Practice</journal-title></journal-title-group><issn>2993-9690</issn><eissn>2993-9704</eissn><publisher><publisher-name>Art and Technology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.61369/MRP.2026090029</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title>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</title><url>https://artdesignp.com/journal/MRP/4/9/10.61369/MRP.2026090029</url><author>陆妍,宋吉涛</author><pub-date pub-type="publication-year"><year>2026</year></pub-date><volume>4</volume><issue>9</issue><history><date date-type="pub"><published-time>2026-09-20</published-time></date></history><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&amp;ldquo;肠道氧化应激累积- 屏障功能崩溃- 菌群代谢物易位&amp;rdquo;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&amp;ldquo;生物钟- 代谢耦合&amp;rdquo;理论，探讨恢复昼夜节律与调整饮食习惯的联合干预策略。</abstract><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</keywords></article-meta></front><body/><back><ref-list><ref id="B1" content-type="article"><label>1</label><element-citation publication-type="journal"><p>[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.</p><pub-id pub-id-type="doi"/></element-citation></ref></ref-list></back></article>
