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©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 21, 2025; 31(47): 113205
Published online Dec 21, 2025. doi: 10.3748/wjg.v31.i47.113205
Published online Dec 21, 2025. doi: 10.3748/wjg.v31.i47.113205
Tumor necrosis factor-α promotes abnormal glucose metabolism after acute pancreatitis by inducing islet β-cell apoptosis via Bax/Bcl-2/caspase-3 signaling pathway
Hai-Feng Chen, Chen Gong, Jian-Xin Zhu, Department of Gastroenterology, Taicang Affiliated Hospital of Soochow University (The First People’s Hospital of Taicang), Taicang 215400, Jiangsu Province, China
Ting-Ting Wang, Department of Nephrology, Taicang Affiliated Hospital of Soochow University (The First People’s Hospital of Taicang), Taicang 215400, Jiangsu Province, China
Wei-Ping Li, Department of Gastrointestinal Surgery, Taicang Affiliated Hospital of Soochow University (The First People’s Hospital of Taicang), Suzhou 215400, Jiangsu Province, China
Co-first authors: Hai-Feng Chen and Chen Gong.
Co-corresponding authors: Ting-Ting Wang and Wei-Ping Li.
Author contributions: Chen HF and Gong C contributed to the writing of the manuscript and they contributed equally to this work as co-first authors. Chen HF and Li WP conceptualized and designed the research study; Zhu JX developed the concept for the article and provided writing ideas; Wang TT and Li WP acquired and analyzed data from experiments and contributed equally to this work as co-corresponding authors. All authors read and agreed to the published version of the manuscript.
Supported by Taicang Science and Technology Program, No. TC2021JCYL21; “National Tutor System” Training Program for Health Youth Key Talents in Suzhou, No. Qngg2023042; and Suzhou Science and Technology Bureau, No. SYW2024152.
Institutional review board statement: This study was approved by the Institutional Review Board of the First People’s Hospital of Taicang (No. KY-2022-001).
Institutional animal care and use committee statement: All animal procedures were approved by Institutional Animal Care and Use Committee at Lanly Bioscience (Suzhou) Co., Ltd. (No. IACUC-221220).
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Data sharing statement: The manuscript contains all data supporting the reported results.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Wei-Ping Li, Department of Gastrointestinal Surgery, Taicang Affiliated Hospital of Soochow University (The First People’s Hospital of Taicang), No. 58 South Chang
Received: August 19, 2025
Revised: September 29, 2025
Accepted: November 7, 2025
Published online: December 21, 2025
Processing time: 122 Days and 21.1 Hours
Revised: September 29, 2025
Accepted: November 7, 2025
Published online: December 21, 2025
Processing time: 122 Days and 21.1 Hours
Core Tip
Core Tip: Acute pancreatitis (AP) often leads to abnormal glucose metabolism (AGM). This study investigated the role of tumor necrosis factor-α (TNF-α) in AP-associated AGM, and our results showed elevated TNF-α promoted β-cell apoptosis via the Bax/Bcl-2/caspase-3 signaling pathway, contributing to AGM. Inhibiting TNF-α reduced apoptosis and improved AGM, indicating its potential as a therapeutic target for preventing AGM after AP.