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Sustained secretory demand leads to intracellular Ca 2+ overload, mitochondrial dysfunction, heightened oxidative stress, and progressive -cell exhaustion (Figure 2C highlights the immunological arm of this axis, showing how SCFAs and related metabolites polarize macrophages toward an M2-like phenotype, promote Treg differentiation and increase IL-10/TGF- production, thereby dampening systemic and islet inflammation and indirectly preserving -cell function

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