Copyright: ©Author(s) 2026.
World J Diabetes. May 15, 2026; 17(5): 118754
Published online May 15, 2026. doi: 10.4239/wjd.v17.i5.118754
Published online May 15, 2026. doi: 10.4239/wjd.v17.i5.118754
Figure 1 Mechanisms of macrophage-driven β-cell impairment in obesity/T2DM islets.
Activated macrophages release interleukin-1 β (inducible nitric oxide synthase/nitric oxide axis), galectin-3 (Ca2+ dysregulation), prostaglandin E2 (cyclic adenosine monophosphate reduction), and exosomal miR-212-5p (sirtuin 2 suppression), and form tunneling nanotubes to deplete insulin granules, collectively impairing Glucose-stimulated insulin secretion and β-cell viability. (by figdraw.com). IL-1β: Interleukin-1β; iNOS: Inducible nitric oxide synthase; NO: Nitric oxide; Gal3: Galectin-3; PGE2: Prostaglandin E2; SIRT2: Sirtuin 2; GSIS: Glucose-stimulated insulin secretion.
- Citation: Wang YJ, Wang SY, Li ZM, Zhao MY, Zhou M, Xie CY, Wang JA, Xu B, Yang GH, Liu Y, Xu TC. Unlocking pancreatic metabolic memory: Can early interventions reverse obesity and block diabetes before it strikes? World J Diabetes 2026; 17(5): 118754
- URL: https://www.wjgnet.com/1948-9358/full/v17/i5/118754.htm
- DOI: https://dx.doi.org/10.4239/wjd.v17.i5.118754