高脂血症性急性胰腺炎合并脂肪性肝病的分子机制

董说; 王莹; 王希望; 金晶晶; 魏凯; 王晓

doi:10.12449/JCH260333

高脂血症性急性胰腺炎合并脂肪性肝病的分子机制

DOI: 10.12449/JCH260333

董说^{1, 2, 3},
王莹^{1, 2, 3},
王希望^{1, 2, 3},
金晶晶^{1, 2, 3},
魏凯^{1, 2, 3},
王晓^{1, 3, , ,}

1.
河南中医药大学第一附属医院脾胃肝胆科，郑州 450000
2.
河南中医药大学第一临床医学院，郑州 450000
3.
中西医防治重大疾病河南省协同创新中心，郑州 450000

基金项目:

河南中医药大学“双一流”创建工程中医学学科项目 (HSRP-DFCTCM-2023-1-08);

河南省中医药科学研究专项课题 (2019JDZX2050)

利益冲突声明：本文不存在任何利益冲突。

作者贡献声明：董说、王莹对研究思路和文章撰写有关键贡献；王希望、金晶晶、魏凯参与修改文章；王晓对文章关键内容进行指导与修改。

详细信息

通信作者:
王晓， wangxiao1113@126.com （ORCID： 0000-0002-4676-2487）

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出版历程
- 收稿日期: 2025-07-29
- 录用日期: 2025-09-03
- 出版日期: 2026-03-25

Molecular mechanisms of hyperlipidemic acute pancreatitis comorbid with fatty liver disease

Shuo DONG^{1, 2, 3},
Ying WANG^{1, 2, 3},
Xiwang WANG^{1, 2, 3},
Jingjing JIN^{1, 2, 3},
Kai WEI^{1, 2, 3},
Xiao WANG^{1, 3
, ,
,}

1.
Spleen，Stomach and Hepatobiliary Department，The First Affiliated Hospital of Henan University of Chinese Medicine，Zhengzhou 450000，China
2.
The First Clinical Medical College of Henan University of Chinese Medicine，Zhengzhou 450000，China
3.
Henan Provincial Collaborative Innovation Center for Prevention and Treatment of Major Diseases with Chinese and Western Medicine，Zhengzhou 450000，China

Research funding:

Project of Traditional Chinese Medicine Discipline in the “Double First-Class” Initiative of Henan University of Chinese Medicine (HSRP-DFCTCM-2023-1-08);

Special Project of Traditional Chinese Medicine in Henan Province (2019JDZX2050)

More Information

Corresponding author: WANG Xiao， wangxiao1113@126.com （ORCID： 0000-0002-4676-2487）

摘要

摘要: 高脂血症性急性胰腺炎和脂肪性肝病均与脂质代谢紊乱有关，二者在临床上常合并存在。其发生机制涉及高甘油三酯血症、代谢综合征、肥胖及胰岛素抵抗等多种因素的相互作用，这些因素可形成恶性循环，共同促进疾病进展。高脂血症性急性胰腺炎在临床上具有病情重、并发症发生率高、病死率高及易复发等特点，若治疗延误，易导致多器官损伤，甚至引发多器官功能衰竭，严重威胁患者生命。本文从高脂血症性急性胰腺炎合并脂肪性肝病相关的多种信号调控通路入手，分析并探讨二者协同致病的潜在分子机制，从而为该共患病的早期预防与治疗提供一定的参考依据。
- 胰腺炎 /
- 高脂血症 /
- 脂肪肝 /
- 信号通路
Abstract: Both hyperlipidemic acute pancreatitis and fatty liver disease are associated with lipid metabolism disorders and are commonly comorbid with each other in clinical practice. The pathogenesis of such comorbidity involves the interaction between multiple factors such as hypertriglyceridemia， metabolic syndrome， obesity， and insulin resistance， and these factors may form a vicious cycle and jointly promote disease progression. In clinical practice， hyperlipidemic acute pancreatitis is characterized by severe disease conditions， a high incidence rate of complications， a high mortality rate， and a tendency for recurrence， and it can easily lead to multi-organ damage and even multiple organ failure without timely treatment， posing a serious threat to the life of patients. Starting from the various signaling pathways associated with hyperlipidemic acute pancreatitis comorbid with fatty liver disease， this article discusses the potential molecular mechanisms of synergistic pathogenesis between hyperlipidemic acute pancreatitis and fatty liver disease， so as to provide a reference for the early prevention and treatment of such comorbidity.
- Pancreatitis /
- Hyperlipidemias /
- Fatty Liver /
- Signaling Pathway

HTML全文

注： TG，甘油三酯；ROS，活性氧；FFA，游离脂肪酸；NLRP3，核苷酸结合寡聚结构域样受体家族热蛋白结构域相关蛋白3；IL-18，白细胞介素18；IL-1β，白细胞介素1β；FLD，脂肪性肝病；HLAP，高脂血症性急性胰腺炎。

图 1 HLAP合并FLD中NLRP3炎症小体通路分子机制

Figure 1. Molecular mechanism of the NLRP3 inflammasome pathway in HLAP combined with FLD

下载: 全尺寸图片幻灯片

注： PI3K，磷脂酰肌醇3-激酶；Akt，蛋白激酶B；mTOR，哺乳动物雷帕霉素靶蛋白；mTORC1，哺乳动物雷帕霉素靶蛋白复合体1；TG，甘油三酯；FLD，脂肪性肝病；HLAP，高脂血症性急性胰腺炎。

图 2 HLAP合并FLD中PI3K/Akt通路的分子机制

Figure 2. Molecular mechanism of the PI3K/Akt pathway in HLAP combined with FLD

下载: 全尺寸图片幻灯片

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