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Thyrotropin, hyperthyroidism, and bone mass

(54) found that administering GIPR antagonist to healthy humans reduced postprandial insulin secretion and increased glucose excursions more than administering GLP-1R antagonist (GLP-1RA), indicating that endogenous GIP may play a more significant role in stimulating insulin secretion and reducing postprandial plasma glucose excursions compared to endogenous GLP-1

[3] Firstly, they stimulate the release of insulin from the pancreatic beta cells in response to elevated blood glucose levels, thereby lowering blood sugar