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Chronic inflammation in diabetic wounds leads to T-cell accumulation and subsequently elevated levels of C-C motif chemokine receptor 4 and TNF-α, thereby significantly impacting the immune response and increasing susceptibility to opportunistic pathogens in wounds (74–76)

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In contrast, PDK2 inhibition in astrocytes significantly attenuates diabetes-induced hypothalamic inflammation, lowers lactate levels, and normalizes abnormal feeding behavior (Rahman et al., 2020)