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• W2019439059 abstract "BackgroundExcessive myocyte apoptosis and impaired neoangiogenesis contribute to the propensity for diabetic patients to develop heart failure following myocardial infarction. Stromal derived factor-1 (SDF-1) is an anti-apoptotic and pro-angiogenic chemokine that is elaborated in response to ischemic injury but is rapidly degraded by di-peptidyl peptidase-4 (DPP-4). Because DPP-4 also degrades the glucose lowering incretin, GLP-1, inhibitors of DPP-4 are currently marketed for the treatment of type 2 diabetes. Importantly, GLP-1, has also been shown to exert cardiotropic effects, increasing cardiac contractility in acute and chronic heart failure. We speculated that DPP-4 inhibition may confer benefit following myocardial infarction (MI) in the diabetic setting as a consequence of enhanced SDF-1 availability rather than potentiating GLP-1. To test this hypothesis we compared the DPP-4 inhibitor, saxagliptin with the GLP-1 agonist, liraglutide. To ensure that any effects would be glucose-independent, we studied experimental MI in a model of type 1, rather than type 2 diabetes.MethodsFischer F344 rats with streptozotocin (STZ)-diabetes were randomized to receive the DPP-4 inhibitor, saxagliptin (10 mg/kg/d), liraglutide (0.2mg/kg/sc/BID) or vehicle. Two weeks later animals underwent experimental MI, induced by ligation of the left anterior descending coronary artery. Cardiac function, assessed by conductance catheterization and echocardiography were examined 4 weeks post-MI.ResultsAll animals receiving STZ became diabetic (mean HbA1c >10%, P=NS between groups). MI size, 2 days post LAD ligation was similar in both treated and untreated MI groups as were systolic BP and heart size (indexed to body weight). When compared with untreated post-MI rats, those receiving saxagliptin had lower lung weight (indexed to body weight, p < 0.05), improved fractional shortening (p < 0.05) and better diastolic function in both early and late phases as measured by Tau and the slope of the end diastolic pressure volume relationship, respectively (p < 0.05 for both). By contrast, liraglutide-treated animals closely resembled those that had received vehicle.ConclusionTabled 1 BackgroundExcessive myocyte apoptosis and impaired neoangiogenesis contribute to the propensity for diabetic patients to develop heart failure following myocardial infarction. Stromal derived factor-1 (SDF-1) is an anti-apoptotic and pro-angiogenic chemokine that is elaborated in response to ischemic injury but is rapidly degraded by di-peptidyl peptidase-4 (DPP-4). Because DPP-4 also degrades the glucose lowering incretin, GLP-1, inhibitors of DPP-4 are currently marketed for the treatment of type 2 diabetes. Importantly, GLP-1, has also been shown to exert cardiotropic effects, increasing cardiac contractility in acute and chronic heart failure. We speculated that DPP-4 inhibition may confer benefit following myocardial infarction (MI) in the diabetic setting as a consequence of enhanced SDF-1 availability rather than potentiating GLP-1. To test this hypothesis we compared the DPP-4 inhibitor, saxagliptin with the GLP-1 agonist, liraglutide. To ensure that any effects would be glucose-independent, we studied experimental MI in a model of type 1, rather than type 2 diabetes. Excessive myocyte apoptosis and impaired neoangiogenesis contribute to the propensity for diabetic patients to develop heart failure following myocardial infarction. Stromal derived factor-1 (SDF-1) is an anti-apoptotic and pro-angiogenic chemokine that is elaborated in response to ischemic injury but is rapidly degraded by di-peptidyl peptidase-4 (DPP-4). Because DPP-4 also degrades the glucose lowering incretin, GLP-1, inhibitors of DPP-4 are currently marketed for the treatment of type 2 diabetes. Importantly, GLP-1, has also been shown to exert cardiotropic effects, increasing cardiac contractility in acute and chronic heart failure. We speculated that DPP-4 inhibition may confer benefit following myocardial infarction (MI) in the diabetic setting as a consequence of enhanced SDF-1 availability rather than potentiating GLP-1. To test this hypothesis we compared the DPP-4 inhibitor, saxagliptin with the GLP-1 agonist, liraglutide. To ensure that any effects would be glucose-independent, we studied experimental MI in a model of type 1, rather than type 2 diabetes. MethodsFischer F344 rats with streptozotocin (STZ)-diabetes were randomized to receive the DPP-4 inhibitor, saxagliptin (10 mg/kg/d), liraglutide (0.2mg/kg/sc/BID) or vehicle. Two weeks later animals underwent experimental MI, induced by ligation of the left anterior descending coronary artery. Cardiac function, assessed by conductance catheterization and echocardiography were examined 4 weeks post-MI. Fischer F344 rats with streptozotocin (STZ)-diabetes were randomized to receive the DPP-4 inhibitor, saxagliptin (10 mg/kg/d), liraglutide (0.2mg/kg/sc/BID) or vehicle. Two weeks later animals underwent experimental MI, induced by ligation of the left anterior descending coronary artery. Cardiac function, assessed by conductance catheterization and echocardiography were examined 4 weeks post-MI. ResultsAll animals receiving STZ became diabetic (mean HbA1c >10%, P=NS between groups). MI size, 2 days post LAD ligation was similar in both treated and untreated MI groups as were systolic BP and heart size (indexed to body weight). When compared with untreated post-MI rats, those receiving saxagliptin had lower lung weight (indexed to body weight, p < 0.05), improved fractional shortening (p < 0.05) and better diastolic function in both early and late phases as measured by Tau and the slope of the end diastolic pressure volume relationship, respectively (p < 0.05 for both). By contrast, liraglutide-treated animals closely resembled those that had received vehicle. All animals receiving STZ became diabetic (mean HbA1c >10%, P=NS between groups). MI size, 2 days post LAD ligation was similar in both treated and untreated MI groups as were systolic BP and heart size (indexed to body weight). When compared with untreated post-MI rats, those receiving saxagliptin had lower lung weight (indexed to body weight, p < 0.05), improved fractional shortening (p < 0.05) and better diastolic function in both early and late phases as measured by Tau and the slope of the end diastolic pressure volume relationship, respectively (p < 0.05 for both). By contrast, liraglutide-treated animals closely resembled those that had received vehicle. ConclusionTabled 1" @default.
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• W2019439059 title "776 DPP-4 Inhibition Improves Cardiac Function Following Experimental Myocardial Infarction: Potential Non-Glp-1 Mediated Effects" @default.
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