We are analyzing https://link.springer.com/article/10.1007/s00210-011-0665-3.

Title:
DPP4 deficiency preserves cardiac function via GLP-1 signaling in rats subjected to myocardial ischemia/reperfusion | Naunyn-Schmiedeberg's Archives of Pharmacology
Description:
Dipeptidyl peptidase-4 (DPP4) enzyme inhibition has been reported to increase plasma glucagon-like peptide-1 (GLP-1) level for controlling postprandial glucose concentration. Both DPP4 inhibitors and GLP-1 analog have been approved for antihyperglycemic agents. In addition to the insulinotropic effect, GLP-1 signaling was reported to modulate cardiac function. DPP4 inhibition was shown to improve survival rate after myocardial infarction in mice, but the precise mechanism remains unknown. We aimed to compare the cardiovascular responses of ischemia/reperfusion (I/R) between wild-type and DPP4-deficient rats and investigate the underlying mechanism. Rats were subjected to 45 min of coronary artery occlusion, followed by reperfusion for 2 h. Cardiac function was characterized by analyzing pressure–volume loops. As compared to wild-type rats, after I/R, DPP4-deficient rats had better cardiac performance in association with less infarct size and cardiac injury markers (LDH, ANP, and BNP), which could be attenuated by exendin-(9–39), a GLP-1 receptor antagonist. Exendin-(9–39) could diminish the increased phosphorylation levels of myocardial AKT and GSK-3β as well as the higher expression of GLUT4 in post-infarcted DPP4-deficient rats. However, exendin-(9–39) could not completely abrogate the less infarct size in DPP4-deficient rats as compared with that in wild-type rats, implicating the involvement of GLP-1 receptor-independent pathway. In summary, this study demonstrated that the benefit of cardiac protective action against I/R injury was demonstrated in DPP4-deficient rats, which is mediated through both GLP-1 receptor-dependent and receptor-independent mechanisms.
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Keywords {🔍}

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Topics {✒️}

wen-pin chen & ming-jai su analyzing pressure–volume loops month download article/chapter post-infarcted dpp4-deficient rats cd26/dipeptidyl peptidase iv noyan-ashraf mh nitric oxide-dependent mechanisms gsk-3beta-mediated myocardial protection glycogen synthase kinase-3beta ming-jai su myocardial ischemia/reperfusion injury dipeptidyl peptidase iv phosphoinositide 3-kinase-dependent mechanism pi3k/akt pathway t-cell immune response pacing-induced dilated cardiomyopathy p38alpha map kinase-mediated moonlighting protein cd26/dppiv article naunyn-schmiedeberg' arterial blood pressure left ventricular dysfunction cd26/dpp-iv inhibition related subjects modulate cardiac function glp-1 receptor-independent pathway full article pdf myocardial ischemia/reperfusion reperfusion induced injury ischemia/reperfusion injury ischemia-reperfusion injury akt promotes survival privacy choices/manage cookies author information authors cardiac injury markers peptide-1 receptor agonist ischemia/reperfusion ldh cardiac protective action heart rate induced van noorden cj article ku peptide-1 increases camp check access instant access glp-1 receptor-dependent wild-type rats peptide 1 receptor-dependent cardiac function dpp4-deficient rats emerging cardiovascular actions coronary artery disease

Questions {❓}

Grieve DJ, Cassidy RS, Green BD (2009) Emerging cardiovascular actions of the incretin hormone glucagon-like peptide-1: potential therapeutic benefits beyond glycaemic control?
Michel MC, Fliers E, Van Noorden CJ (2008) Dipeptidyl peptidase IV inhibitors in diabetes: more than inhibition of glucagon-like peptide-1 metabolism?

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