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Mechanistically, GLP-1R activation alleviates OA by fostering chondrocyte anabolic metabolism while inhibiting catabolism, safeguarding chondrocytes from endoplasmic reticulum stress and apoptosis, and displaying anti-inflammatory and antioxidant properties [15,16,17]

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Beyond homeostatic regulation, current evidence also supports the role of GLP-1 in hedonic feeding, which is driven by palatability rather than physiological need [52], and involves neurobiological pathways related to mesolimbic dopamine transmission and mechanisms related to reward processing [53]