ArticleWorld journal of gastroenterology2025
Tumor necrosis factor-α promotes abnormal glucose metabolism after acute pancreatitis by inducing islet β-cell apoptosis
Article in World journal of gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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5 authors.
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Abstract
backgroundTumor 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.
aimTo investigate the role of TNF-α in AP-associated AGM and its effects on islet β-cell apoptosis, focusing on the underlying molecular mechanisms.
methodsClinical data were collected to assess AGM's incidence and identify the characteristics in 369 AP patients.
resultsAGM 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 inflammation severity. Similar findings of β-cell apoptosis were confirmed in the mouse model. TNF-α 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
conclusionTNF-α contributes to β-cell apoptosis and AGM in AP through the Bax/Bcl-2/caspase-3 signaling pathway, suggesting TNF-α as a potential therapeutic target for preventing AP-associated AGM.
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