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In contrast to GLP-1, the incretin hormone glucose-dependent insulinotropic polypeptide (GIP) received little attention as a pharmacological target, because of conflicting observations that argue activation or inhibition of the GIP receptor (GIPR) provides beneficial effects on systemic metabolism

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the rates of insulin initiation observed for both semaglutide and DPP4i users at the end of the study were markedly lower than what has been reported in the literature [31]