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DPP-4i and GLP-1RAs are able to enhance vasodilation by increasing nitric oxide production, promote myocyte glucose uptake, and increase coronary flow, thus providing cardioprotective effects during the acute phase of ischemic heart diseases [85,86,87,88]

These findings raise the possibility that loss of enterocyte DPP-4 in the context of HFD feeding upregulates pathways converging on enhanced TRL secretion