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首页|期刊导航|中国实用内科杂志|胰腺炎的代谢视角——脂代谢异常在胰腺炎及内外分泌并发症中的病理枢纽

胰腺炎的代谢视角——脂代谢异常在胰腺炎及内外分泌并发症中的病理枢纽

王茹澜 张芙蓉 于慧敏 胡良皞 李拓

中国实用内科杂志2026,Vol.46Issue(8):617-624,8.
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中国实用内科杂志2026,Vol.46Issue(8):617-624,8.DOI:10.19538/j.nk2026080101

胰腺炎的代谢视角——脂代谢异常在胰腺炎及内外分泌并发症中的病理枢纽

A metabolic perspective on pancreatitis:dysregulated lipid metabolism as a pathological hub in pancreatitis and exocrine and endocrine complications

王茹澜 1张芙蓉 1于慧敏 1胡良皞 2李拓1

作者信息

  • 1. 上海长征医院内分泌科,上海 200003
  • 2. 上海长海医院消化内科,上海 200433
  • 折叠

摘要

Abstract

Hypertriglyceridemia has emerged as the second leading cause of acute pancreatitis.Circulating overloads of triglycerides and their hydrolytic products,free fatty acids,trigger pancreatic exocrine and endocrine cellular dysfunction and inflammatory infiltration through mechanical obstruction,chemical toxicity,and ectopic lipid deposition,serving as the core pathological hub driving disease aggravation and recurrence.This review systematically elucidates the pathological cascade mediated by dysregulated lipid metabolism,which encompasses inflammation driving,acinar injury,fibrotic remodeling,and malignant transformation,and evaluates the clinical value of lipid metabolism-related biomarkers along with their potential for long-term intervention.It is emphasized that dysregulated lipid metabolism persists throughout the entire disease course.Thus,the clinical paradigm must urgently shift from localized symptomatic management of pancreatitis toward a lipid homeostasis-centered,full-cycle management of pancreatitis syndrome.Correcting lipid disorders through multidisciplinary collaboration is essential to mitigating acute inflammation,preserving exocrine and endocrine functions,and improving long-term outcomes of patients.

关键词

脂代谢异常/胰源性糖尿病/胰腺炎/脂肪浸润/脂肪胰

Key words

dysregulated lipid metabolism/pancreatogenic diabetes/pancreatitis/fatty infiltration/fatty pancreas

分类

医药卫生

引用本文复制引用

王茹澜,张芙蓉,于慧敏,胡良皞,李拓..胰腺炎的代谢视角——脂代谢异常在胰腺炎及内外分泌并发症中的病理枢纽[J].中国实用内科杂志,2026,46(8):617-624,8.

基金项目

国家自然科学基金(82595903) (82595903)

中国实用内科杂志

1005-2194

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