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Clinical review of 369 acute pancreatitis patients assessed AGM incidence and associated characteristics, while in vitro models used lipopolysaccharide-treated 266-6 acinar cells and MIN-6 β-cells, and an in vivo sodium taurocholate mouse model. Measures included proliferation, apoptosis, protein expression, and TNF-α inhibition effects. 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31(47): 113205  \nDOI: 10.3748/wjg.v31.i47.113205 ISSN 1007-9327 (print) ISSN 2219-2840 (online)  \nORIGINAL ARTICLE  \nBasic Study  \nTumor necrosis factor-α promotes abnormal glucose metabolism after acute pancreatitis by inducing islet β-cell apoptosis via Bax/Bcl-2/caspase-3 signaling pathway  \nHai-Feng Chen, Chen Gong, Ting-Ting Wang, Jian-Xin Zhu, Wei-Ping Li  \nSpecialty type: Gastroenterology and hepatology  \nProvenance and peer review:  \nInvited article; Externally peer reviewed.  \nPeer-review model: Single blind  \nPeer-review report’s classification Scientific Quality: Grade B, Grade B  \nNovelty: Grade A, Grade B  \nCreativity or Innovation: Grade B, Grade B  \nScientific Significance: Grade B, Grade B  \nP-Reviewer: Liu Y, MD, PhD, Postdoctoral Fellow, China; Molasy B, MD, PhD, Assistant Professor, Poland  \nReceived: August 19, 2025  \nRevised: September 29, 2025  \nAccepted: November 7, 2025  \nPublished online: December 21, 2025  \nProcessing time: 122 Days and 20.3 Hours  \nHai-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  \nTing-Ting Wang, Department of Nephrology, Taicang Affiliated Hospital of Soochow  \nUniversity (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.  \nCo-corresponding authors: Ting-Ting Wang and Wei-Ping Li.  \nCorresponding author: Wei-Ping Li, Department of Gastrointestinal Surgery, Taicang Affiliated Hospital of Soochow University (The First People’s Hospital of Taicang), No. 58 South Changsheng Road, Suzhou 215400, Jiangsu Province, [China.](China. question12397@163.com)[ question12397@163.com](China. question12397@163.com)  \nAbstract  \nBACKGROUND  \nTumor necrosis factor-α (TNF-α) has been implicated in the development of diabetes following chronic pancreatitis. However, its role in abnormal glucose metabolism (AGM) after acute pancreatitis (AP) and post-pancreatitis diabetes mellitus remains unclear.  \nAIM  \nTo investigate the role of TNF-α in AP-associated AGM and its effects on islet β -cell apoptosis, focusing on the underlying molecular mechanisms.  \nMETHODS  \nClinical data were collected to assess AGM’s incidence and identify the characteristics in 369 AP patients. In vitro, AP models were established using lipopolysaccharide in 266-6 acinar cells and MIN-6 β-cells. Cell proliferation, apoptosis, and protein expression were analyzed using the Cell Counting Kit-8 assay, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, and western blotting. The TNF-α and insulin concentration in co-culture medium was measured by  \n WJG  [https://www.wjgnet.com](https://www.wjgnet.com) 1 December 21, 2025  Volume 31  Issue 47   \nChen HF et al. TNF-α-induced β-cell apoptosis in AGM  \nenzyme-linked immunosorbent assay. In vivo, an AP mouse model was induced using sodium taurocholate, and pancreatic tissues were analyzed through hematoxylin and eosin staining, terminal deoxynucleotidyl transferasedUTP nick-end labeling, and western blotting. TNF-α levels were assessed by enzyme-linked immunosorbent assay. A TNF-α inhibitor was applied to the AP cell model to reassess apoptosis and protein expression.  \nRESULTS  \nAGM occurred in 40.38% of AP patients. Body mass index, severity grade, recurrence frequency, and lung injury were significantly associated with AGM. AP models in 266-6 and MIN-6 cells showed reduced β-cell proliferation, insulin secretion, and increased apoptosis, which correlated with in","cbCaidgnF6a0zdpc","https://ap.wps.com/l/cbCaidgnF6a0zdpc","pdf",6983671,15,"English","# Abstract\n## Background\n## Aim\n## Methods\n## Results\n## Conclusion\n# Key Words\n# Core Tip","[{\"question\":\"What question does the study address about TNF-α and acute pancreatitis?\",\"answer\":\"It examines TNF-α’s role in abnormal glucose metabolism after acute pancreatitis and how it affects islet β-cell apoptosis through molecular mechanisms.\"},{\"question\":\"How was abnormal glucose metabolism assessed in patients and models?\",\"answer\":\"The study collected clinical data to determine AGM incidence and characteristics in 369 acute pancreatitis patients, and used cell and mouse models to evaluate β-cell function and apoptosis.\"},{\"question\":\"What molecular pathway links TNF-α to β-cell apoptosis in this work?\",\"answer\":\"The findings implicate Bax/Bcl-2/caspase-3 signaling, with increased Bax and caspase-3 and decreased Bcl-2 after TNF-α elevation; TNF-α inhibition reverses these patterns.\"}]","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 | PDF",1790565308,38]