{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,11]],"date-time":"2026-11-11T15:55:17Z","timestamp":1794412517615,"version":"4.9.0"},"reference-count":45,"publisher":"Baishideng Publishing Group Inc.","issue":"47","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["World J Gastroenterol"],"abstract":"<jats:p>BACKGROUND<\/jats:p>\n                  <jats:p>Tumor necrosis factor-\u03b1 (TNF-\u03b1) 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.<\/jats:p>\n                  <jats:p>AIM<\/jats:p>\n                  <jats:p>To investigate the role of TNF-\u03b1 in AP-associated AGM and its effects on islet \u03b2-cell apoptosis, focusing on the underlying molecular mechanisms.<\/jats:p>\n                  <jats:p>METHODS<\/jats:p>\n                  <jats:p>Clinical data were collected to assess AGM\u2019s 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 \u03b2-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-\u03b1 and insulin concentration in co-culture medium was measured by enzyme-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 transferase dUTP nick-end labeling, and western blotting. TNF-\u03b1 levels were assessed by enzyme-linked immunosorbent assay. A TNF-\u03b1 inhibitor was applied to the AP cell model to reassess apoptosis and protein expression.<\/jats:p>\n                  <jats:p>RESULTS<\/jats:p>\n                  <jats:p>AGM 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 \u03b2-cell proliferation, insulin secretion, and increased apoptosis, which correlated with inflammation severity. Similar findings of \u03b2-cell apoptosis were confirmed in the mouse model. TNF-\u03b1 levels were significantly elevated in AP models, with higher levels in severe inflammation. Increased Bax and caspase-3 expression and decreased Bcl-2 expression were observed in both in vitro  and in vivo  models. These changes intensified with increasing inflammation. TNF-\u03b1 inhibition reduced apoptosis and altered protein expression patterns, decreasing Bax and caspase-3, while increasing Bcl-2 in MIN-6 cells.<\/jats:p>\n                  <jats:p>CONCLUSION<\/jats:p>\n                  <jats:p>TNF-\u03b1 contributes to \u03b2-cell apoptosis and AGM in AP through the Bax\/Bcl-2\/caspase-3 signaling pathway, suggesting TNF-\u03b1 as a potential therapeutic target for preventing AP-associated AGM.<\/jats:p>","DOI":"10.3748\/wjg.v31.i47.113205","type":"journal-article","created":{"date-parts":[[2025,12,19]],"date-time":"2025-12-19T01:48:29Z","timestamp":1766108909000},"source":"Crossref","is-referenced-by-count":7,"title":["Tumor necrosis factor-\u03b1 promotes abnormal glucose metabolism after acute pancreatitis by inducing islet \u03b2-cell apoptosis\n                    <i>via<\/i>\n                    Bax\/Bcl-2\/caspase-3 signaling 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