Pancreatic injury and glucose metabolism dysfunction: The central role of inflammatory signaling and islet β-cell apoptosis

doi:10.4239/wjd.117159

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World Journal of Diabetes

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1948-9358

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.

World J Diabetes. Sep 15, 2026; 17(9): 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, Ying Zhang, Chang-Quan Liu, Hong-Jin Chen, Ai-Fang Wang

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. wangaifang19832024@163.com

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

Abstract

Acute pancreatitis is an inflammatory disorder of the pancreas and is closely associated with substantial risks of long-term metabolic dysfunctions, particularly abnormal glucose metabolism and post-pancreatitis diabetes mellitus. A comprehensive understanding of the underlying molecular mechanisms is essential to inform effective clinical intervention. A recent study by Chen et al, published in World Journal of Gastroenterology, provided valuable insights by establishing that tumor necrosis factor-α can induce pancreatic β-cell apoptosis through the Bax/Bcl-2/caspase-3 pathway, revealing a direct inflammatory link to abnormal glucose metabolism following acute pancreatitis. The current commentary critically evaluated the mechanistic interplay between pancreatic injury and inflammatory signaling in the disruption of glucose homeostasis. This study analyzed the clinical implications of these pathways for early diagnosis and management of post-pancreatitis diabetes mellitus. Furthermore, the translational potential of targeting specific inflammatory mediators to preserve β-cell mass and function was discussed. Emerging therapeutic strategies aimed at mitigating pancreatic injury by regulating glucose metabolism and inflammatory responses were also evaluated. The commentary identified persistent research gaps and proposed future directions to translate mechanistic insights into improved patient outcomes.

Keywords: Acute pancreatitis; Glucose metabolism; β-cell apoptosis; Tumor necrosis factor-α; Bax/Bcl-2/caspase-3 pathway; Post-pancreatitis diabetes mellitus

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.