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The tryptophan-kynurenine pathway functions as a stress-activated metabolic system that diverts tryptophan from serotonin synthesis toward kynurenic acid production, which acts as a glutamate receptor antagonist and may contribute to anxiety pathophysiology through altered glutamatergic neurotransmission (Butler et al., 2022)

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In addition to mitochondrial OxS (as detailed below), there are numerous sources of endogenous OxS (e.g., inflammatory responses) that can be relevant to T2D progression [87]