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      Cardiovascular actions of incretin-based therapies.

      Circulation Research
      Animals, Blood Glucose, metabolism, Cardiovascular System, drug effects, physiopathology, Diabetes Mellitus, Type 2, blood, complications, Diabetic Angiopathies, drug therapy, Dipeptidyl Peptidase 4, Disease Models, Animal, Enzyme Inhibitors, pharmacology, Humans, Incretins, therapeutic use, Lipid Metabolism, Mice, Receptors, Glucagon, agonists, Treatment Outcome

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          Abstract

          Glucagon-like peptide-1 receptor (GLP-1R) agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors represent 2 distinct classes of incretin-based therapies used for the treatment of type 2 diabetes mellitus. Activation of GLP-1R signaling or inhibition of DPP-4 activity produces a broad range of overlapping and unique cardiovascular actions. Native GLP-1 regulates cardiovascular biology via activation of the classical GLP-1R, or through GLP-1(9-36), a cardioactive metabolite generated by DPP-4-mediated cleavage. In contrast, clinically approved GLP-1R agonists are not cleaved to GLP-1(9-36) and produce the majority of their actions through the classical GLP-1R. The cardiovascular mechanisms engaged by DPP-4 inhibition are more complex, encompassing increased levels of intact GLP-1, reduced levels of GLP-1(9-36), and changes in levels of numerous cardioactive peptides. Herein we review recent experimental and clinical advances that reveal how GLP-1R agonists and DPP-4 inhibitors affect the normal and diabetic heart and coronary vasculature, often independent of changes in blood glucose. Improved understanding of the complex science of incretin-based therapies is required to optimize the selection of these therapeutic agents for the treatment of diabetic patients with cardiovascular disease. © 2014 American Heart Association, Inc.

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