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These macrophages, particularly the pro-inflammatory Macrophage, pro-inflammatory phenotype (M1) phenotype, secrete cytokines such as C-C motif ligand 2 (CCL2) and transforming growth factor beta (TGF-\u03b2), which disrupt pancreatic \u03b2-cell function and impair insulin secretion. Conversely, anti-inflammatory Macrophage, anti-inflammatory phenotype (M2) macrophages contribute to tissue repair but may also promote fibrotic changes under prolonged metabolic stress. Pancreatic macrophages are activated under high-fat diet conditions, promoting inflammation and impairing \u03b2-cell function through the SUCLA2-HIF-1\u03b1 axis and mechanistic Target of Rapamycin Complex 1 (mTORC1)\/PD-1 pathway, thereby establishing a self-perpetuating \"metabolic-immunosuppressive\" vicious cycle. Targeted intervention strategies against macrophages\u2014such as SUCLA2 inhibitors can ameliorate metabolic dysregulation. Meanwhile, exosome-mediated interorgan communication [e.g. , via  microRNA-155 (miR-155) and miR-30a] offers novel insights for multi-system synergistic therapies. Understanding the mechanisms by which macrophages mediate metabolic dysregulation in the pancreas under obese conditions provides critical insights into the pathogenesis of obesity-related pancreatic disorders.<\/jats:p>","DOI":"10.4331\/wjbc.v16.i4.109509","type":"journal-article","created":{"date-parts":[[2025,12,4]],"date-time":"2025-12-04T02:52:22Z","timestamp":1764816742000},"source":"Crossref","is-referenced-by-count":3,"title":["Macrophage-mediated metabolic dysregulation in the pancreas: Insights from 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