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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 (Wang et al., 2023)

Hypoxia inhibits RANKL-induced ferritinophagy and protects osteoclasts from ferroptosis

Several mutations have been identified

doi: 10.23812/20-411-L

UV exposure, pollution, poor diet, stress all of these create free radicals that damage skin cells