Macrophage-mediated metabolic dysregulation in the pancreas: Insights from obesity

Figure 1 Regulatory mechanisms of pancreatic macrophage modulation in obesity pathogenesis. The figure illustrates the pathological mechanisms by which pancreatic macrophages, upon stimulation, undergo various pathological responses that ultimately lead to pancreatic fibrosis. TGF-β: Transforming growth factor beta; TNF-α: Tumor necrosis factor alpha; NF-κB: Nuclear factor-kappaB.

Figure 2 Role of pancreatic macrophages in obesity-associated metabolic dysregulation. This figure delineates the pathway-mediated process by which islet macrophages polarize into M1 and M2 phenotypes under inflammatory conditions, secreting pro-inflammatory cytokines that ultimately lead to β-cell loss. CCL2: Chemokine (C-C Motif) Ligand 2; HIF-1α: Hypoxia-inducible factor-1 alpha; 12-LOX: 12-lipoxygenase; SUCLA2: Succinate-CoA ligase ADP-forming beta subunit; TGF-β: Transforming growth factor-beta; TNF-α: Tumor necrosis factor-alpha; IL-1β: Interleukin-1 beta