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The therapeutic mechanism of GLP-1 RAs in this population primarily involves overcoming impaired sensitivity through pharmacological receptor stimulation [53]

binds GLP-1 receptors on pancreatic -cells (stimulating glucose-dependent insulin secretion), -cells (suppressing glucagon), gastrointestinal tract (slowing gastric emptying), and hypothalamic neurons (suppressing appetite and food intake via arcuate nucleus signaling)

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