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Results We screened 10,670 studies and ultimately identified 5 eligible studies, encompassing 719 patients

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Physiological Effects Semaglutide exerts its therapeutic benefits through multiple complementary mechanisms: Enhanced Insulin Secretion: Stimulates glucose-dependent insulin release from pancreatic beta cells, improving postprandial glucose control[3][4] Glucagon Suppression: Inhibits glucagon release, reducing hepatic glucose production and improving fasting blood glucose levels[3][4] Delayed Gastric Emptying: Slows the movement of food from the stomach to the small intestine, reducing postprandial glucose excursions and promoting satiety[4][5] Appetite Reduction: Directly affects the central nervous system to decrease food intake and energy consumption[4][5] Improved Metabolic Flexibility: Enhances the body's ability to switch between energy substrates based on availability[2] At the cellular level, semaglutide primarily operates through the AMPK (AMP-activated protein kinase) pathway, which regulates cellular energy homeostasis and improves insulin sensitivity

However, the role of GLP-1R in the pathological process of OA is unclear