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This is explained by a shift in receptor subtype-specificity toward enhanced activation of CC-motif-chemokin-receptor 5 (CCR5) ( in vitro and in vivo in mice, by acting most probably through the intestinal glucose transporter SGLT1 ( Eotaxin/CCL11 Eotaxin mediates mobilization of eosinophils into the bloodstream, which was shown to be increased in DPP4-deficient F344 rats ( DPP4 as a drug target for the treatment of T2DM Deactivation of DPP4 Enzymatic Activity DPP4 inhibitors Major DPP4 substrates are the so-called incretin hormones, which are key regulators of post-prandial insulin release

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