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IR can disrupt this NAD + metabolism, diminishing sirtuin activity and weakening mitochondrial function and neuronal cell survival (Figure 1) ( FIGURE 1 6 GLP-1 and incretin mimetics in PD The incretin hormones known as GLP-1 and GIP are released from enteroendocrine L-cells and K-cells in the small intestine in response to nutrient ingestion, where they play a key role in regulating glucose metabolism and maintaining systemic nutrient homeostasis ( (Heloderma suspectum) saliva as a stable GLP-1 mimetic enabled appetite suppression and glycemic control in metabolic disease, driving the development of long-acting GLP-1 analogues and unimolecular agents that co-activate GLP-1 and GIP receptors ( Although direct involvement of GLP-1/GIP system abnormalities in PD remains uncertain, growing evidence shows that incretin-based therapies can improve cognitive function and exert neuroprotective effects, positioning them as promising candidates for treating neurodegenerative disorders ( In PD models, Agonists of GLP-1 receptor have also been shown to restore impaired GLUT expression and stabilize glucose uptake in brain that supports improvement in metabolic flexibility ( GLP-1 receptor agonists (e.g., exenatide, liraglutide, lixisenatide) and dual GLP-1/GIP agonists (e.g., tirzepatide) have been also reported to reduce microglial and astrocytic hyperactivation and suppress the release of inflammatory mediators such as TNF-, IL-1, and NF-B

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