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GIPR activation produces: Additional glucose-dependent insulin secretion (synergistic with GLP-1R on β-cells) Direct effects on adipocyte (fat cell) lipid metabolism, including enhanced lipid uptake and storage dynamics — paradoxically, this appears to contribute to improved metabolic outcomes by improving adipose tissue function rather than simply increasing fat storage Bone metabolism regulation — GIPR is expressed in osteoblasts and osteoclasts and influences bone turnover (research area) Central nervous system effects via hypothalamic GIPR that are distinct from but complementary to GLP-1R appetite circuits The synergy between GIPR and GLP-1R at the β-cell level amplifies insulin secretion beyond what either receptor achieves alone