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In individuals with T2DM, chronic hyperglycemia is known to downregulate GIPR expression and impair GIP-stimulated insulinotropic activity, thereby limiting the efficacy of GIP monotherapy [21]

In my experience, tirzepatide patients hit plateau less frequently and later in their treatment course than semaglutide patients

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The framework below summarizes evidence-based interventions with their documented mechanisms and expected timeframes for metabolic adaptation

Understanding your genetic predispositionssuch as variants in GLP1R, GIPR, and FTO genesempowers your healthcare team to personalize not only your semaglutide dose but also your complete medication regimen, including decisions about continuing metformin

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