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Emerging research suggests that hyperglycemia-induced oxidative stress, mitochondrial dysfunction, neuroinflammation, and disrupted insulin signaling are central contributors to DE pathogenesis 5,6

These hypothalamic effects may differ among patients treated with GLP-1 receptor agonists

Negative hormonal regulation of symbiotic nodule development

S2F), suggesting that reduced availability of TCA cycle-derived substrates for oxidative phosphorylation results in decreased basal respiration and SRC

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Adjustments are made based on diagnostic results, recovery demands and individual health goals