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These agents activate the cAMP-PKA signaling cascade in pancreatic -cells 6 , resulting in glucose-dependent insulin secretion, suppression of pancreatic -cell glucagon release, and modulation of gastrointestinal motility through delayed gastric emptying 7

Combined with the theory of GIP being an obesogenic hormone (53), these prior findings have highlighted the potential of GIP receptor antagonism, and today the development of GIP receptor antagonists has also emerged as an attractive therapeutic approach for addressing obesity and cardiovascular diseases (54, 55)

(2025), in Diabetes, Obesity and Metabolism, reported a weighted mean difference of 1.02 kg in lean body mass across 19 RCTs

Every patient responds to treatment a little differently