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GIPR agonism could exert beneficial metabolic effects by enhancing glucose-stimulated insulin secretion, increasing postprandial adipose tissue blood flow and triglyceride storage, and by attenuating weight loss-induced bone loss by decreasing bone resorption and increasing osteoblast activity
In obesity, excessive fat accumulation leads to WAT dysfunction, characterized by altered adipokine secretion, impaired WAT expandability, adipocyte hypertrophy, disrupted lipid metabolism, and increased local and systemic inflammation [4,5,6]