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According to studies, the reduced incretin effect in patients with T2DM may be due to a decrease in the response of -cell to GIP and/or GLP-1 or a decrease in GLP secretion [15, 18, 27, 28]

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Collectively, these molecular mechanisms underscore how genetic susceptibility, epigenetic misregulation, and oxidative stress converge to drive thyroid autoimmunity during pregnancy [70,71,72]

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