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World J Diabetes. Sep 15, 2026; 17(9): 117159
Published online Sep 15, 2026. doi: 10.4239/wjd.117159
Published online Sep 15, 2026. doi: 10.4239/wjd.117159
Pancreatic injury and glucose metabolism dysfunction: The central role of inflammatory signaling and islet β-cell apoptosis
Fang-Fang Qi, Department of Pharmacy, Quzhou Maternal and Child Health Care Hospital, Quzhou 324000, Zhejiang Province, China
Ying Zhang, Hong-Jin Chen, Key Laboratory of Emergency and Trauma, Ministry of Education, The First Affiliated Hospital, Hainan Medical University, Haikou 571199, Hainan Province, China
Ying Zhang, Chang-Quan Liu, Hong-Jin Chen, Center for Tissue Engineering and Stem Cell Research, Translation Medicine Research Center, Guizhou Biomanufacturing Laboratory, Guizhou Medical University, Gui’an 561113, Guizhou Province, China
Ying Zhang, Chang-Quan Liu, Hong-Jin Chen, Department of Pharmacology, School of Basic Medical Sciences, Guizhou Medical University, Gui’an 561113, Guizhou Province, China
Ai-Fang Wang, Department of Endocrinology, The People’s Hospital of Yuhuan (Yuhuan People’s Hospital Health Community Group), Taizhou 317600, Zhejiang Province, China
Co-first authors: Fang-Fang Qi and Ying Zhang.
Co-corresponding authors: Hong-Jin Chen and Ai-Fang Wang.
Author contributions: Qi FF and Zhang Y have made crucial and indispensable contributions towards the completion of literature review and writing as co-first authors; Liu CQ contributed to the literature review, framework development, and writing; Chen HJ and Wang AF contributed to the study design as co-corresponding authors; all authors have approved the final manuscript.
AI contribution statement: During the preparation of this paper, we used two tools, namely GPT-5.4 and Gemini 3 Pro, which are specifically designed for language translation and polishing. The scientific core content of this thesis, including the conceptual framework, literature analysis, data synthesis and interpretation, was entirely conceived and written by the author’s research team. We use AI tools only for language translation and to enhance the fluency and academic tone of the grammar. Additionally, to ensure the highest level of professional rigor and to eliminate any non-academic expressions that AI might introduce, the final manuscript was further reviewed and refined by a professional editing agency. The design of this study, the critical evaluation of the cited literature, and the explanation of the biological mechanisms discussed in this review were all independently completed by the author’s research team. All the charts in the paper were manually designed and created by the author using BioRender.com. These are original scientific illustrations, not images generated by AI.
Supported by National Natural Science Foundation of China, No. 82260567; Science and Technology Program of Guizhou Province, No. ZK[2023]321; Qiankehe Platform Project, No. KXJZ[2024]004; Taizhou Social Development Science and Technology Plan Project, No. 23ywb146; Key Laboratory of Emergency and Trauma (Hainan Medical University), Ministry of Education, No. KLET-202502; Excellent Young Talents Plan of Guizhou Medical University, No.[2023]112; Guizhou Medical University Key Laboratory of Cardiovascular Disease Basic and Clinical Research, No. 2024001; and Start-Up Fund of Guizhou Medical University, No. J2021032.
Conflict-of-interest statement: All authors declare no conflict of interest in publishing the manuscript.
Corresponding author: Ai-Fang Wang, MD, Department of Endocrinology, The People’s Hospital of Yuhuan (Yuhuan People’s Hospital Health Community Group), No. 18 Changle Road, Chengguan, Taizhou 317600, Zhejiang Province, China.
Received: December 1, 2025
Revised: January 6, 2026
Accepted: January 20, 2026
Published online: September 15, 2026
Processing time: 274 Days and 17.1 Hours
Revised: January 6, 2026
Accepted: January 20, 2026
Published online: September 15, 2026
Processing time: 274 Days and 17.1 Hours
Core Tip
Core Tip: This editorial elucidates a key mechanism through which acute pancreatitis contributes to the development of diabetes: Tumor necrosis factor-α triggers islet β-cell apoptosis via the Bax/Bcl-2/caspase-3 pathway. We underscore the central role of this inflammatory axis in post-pancreatitis diabetes mellitus and advocate for targeting tumor necrosis factor-α as a translatable strategy to preserve β-cell mass and prevent diabetes following pancreatic injury.