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Packer recently proposed an intriguing hypothesis that DPP-4 inhibitors potentiate some endogenous peptides, such as stromal cell-derived factor-1, in addition to activation of GLP-1, and that unfavorable effects of those peptides on CV parameters (e.g., inflammation, fibrosis, plaque growth, and sympathetic activation) could prevail against the CV protective effects of GLP-1, possibly leading to worsened CV complications and HF [36, 37]

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