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GIP (glucose-dependent insulinotropic polypeptide) was historically considered primarily a glucose-dependent insulin secretagogue, but tirzepatide's development revealed additional metabolic roles: Central appetite regulation : GIP receptors in the hypothalamus and brainstem contribute to satiety signaling through pathways distinct from GLP-1 Adipose tissue effects : GIP receptors on adipocytes modulate lipid storage and adipokine secretion Beta-cell protection : GIP signaling supports pancreatic beta-cell survival and proliferation Bone metabolism : GIP has anti-resorptive effects on bone, potentially mitigating osteoporosis risk during weight loss GLP-1 receptor agonism provides complementary glucose-lowering and appetite-suppressing effects, as described above

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