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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

GGCT channels Gln flux for GSH synthesis and Glc anaplerosis into the TCA cycle ROS act as signaling molecules that regulate mitochondrial function, with mitochondrial morphology intrinsically linked to core processes, including the TCA cycle and oxidative phosphorylation