Circulating Dipeptidyl Peptidase IV Activity Correlates With Cardiac Dysfunction in Human and Experimental Heart Failure
The present study addresses the hypothesis that the activity of dipeptidyl peptidase IV (DPPIV), an enzyme that inactivates peptides that possess cardioprotective actions, correlates with adverse outcomes in heart failure (HF). The therapeutic potential of DPPIV inhibition in preventing cardiac dysf...
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| Published in | Circulation. Heart failure Vol. 6; no. 5; pp. 1029 - 1038 |
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| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
01.09.2013
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| Subjects | |
| Online Access | Get full text |
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| Abstract | The present study addresses the hypothesis that the activity of dipeptidyl peptidase IV (DPPIV), an enzyme that inactivates peptides that possess cardioprotective actions, correlates with adverse outcomes in heart failure (HF). The therapeutic potential of DPPIV inhibition in preventing cardiac dysfunction is also investigated.
Measurements of DPPIV activity in blood samples obtained from 190 patients with HF and 42 controls demonstrated that patients with HF exhibited an increase of ≈130% in circulating DPPIV activity compared with healthy subjects. Furthermore, an inverse correlation was observed between serum DPPIV activity and left ventricular (LV) ejection fraction in patients with HF. Similarly, radiofrequency LV ablation-induced HF rats displayed higher DPPIV activity in the plasma (≈50%) and heart tissue (≈3.5-fold) compared with sham-operated rats. Moreover, positive correlations were observed between the plasma DPPIV activity and LV end-diastolic pressure and lung congestion. Two days after surgery, 1 group of LV ablation-induced HF rats was treated with the DPPIV inhibitor sitagliptin (40 mg/kg BID) for 6 weeks, whereas the remaining rats were administered water. Hemodynamic measurements demonstrated that radiofrequency LV-ablated rats treated with sitagliptin exhibited a significant attenuation of HF-related cardiac dysfunction, including LV end-diastolic pressure, systolic performance, and chamber stiffness. Sitagliptin treatment also attenuated cardiac remodeling and cardiomyocyte apoptosis and minimized pulmonary congestion.
Collectively, the results presented herein associate circulating DPPIV activity with poorer cardiovascular outcomes in human and experimental HF. Moreover, the results demonstrate that long-term DPPIV inhibition mitigates the development and progression of HF in rats. |
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| AbstractList | The present study addresses the hypothesis that the activity of dipeptidyl peptidase IV (DPPIV), an enzyme that inactivates peptides that possess cardioprotective actions, correlates with adverse outcomes in heart failure (HF). The therapeutic potential of DPPIV inhibition in preventing cardiac dysfunction is also investigated.BACKGROUNDThe present study addresses the hypothesis that the activity of dipeptidyl peptidase IV (DPPIV), an enzyme that inactivates peptides that possess cardioprotective actions, correlates with adverse outcomes in heart failure (HF). The therapeutic potential of DPPIV inhibition in preventing cardiac dysfunction is also investigated.Measurements of DPPIV activity in blood samples obtained from 190 patients with HF and 42 controls demonstrated that patients with HF exhibited an increase of ≈130% in circulating DPPIV activity compared with healthy subjects. Furthermore, an inverse correlation was observed between serum DPPIV activity and left ventricular (LV) ejection fraction in patients with HF. Similarly, radiofrequency LV ablation-induced HF rats displayed higher DPPIV activity in the plasma (≈50%) and heart tissue (≈3.5-fold) compared with sham-operated rats. Moreover, positive correlations were observed between the plasma DPPIV activity and LV end-diastolic pressure and lung congestion. Two days after surgery, 1 group of LV ablation-induced HF rats was treated with the DPPIV inhibitor sitagliptin (40 mg/kg BID) for 6 weeks, whereas the remaining rats were administered water. Hemodynamic measurements demonstrated that radiofrequency LV-ablated rats treated with sitagliptin exhibited a significant attenuation of HF-related cardiac dysfunction, including LV end-diastolic pressure, systolic performance, and chamber stiffness. Sitagliptin treatment also attenuated cardiac remodeling and cardiomyocyte apoptosis and minimized pulmonary congestion.METHODS AND RESULTSMeasurements of DPPIV activity in blood samples obtained from 190 patients with HF and 42 controls demonstrated that patients with HF exhibited an increase of ≈130% in circulating DPPIV activity compared with healthy subjects. Furthermore, an inverse correlation was observed between serum DPPIV activity and left ventricular (LV) ejection fraction in patients with HF. Similarly, radiofrequency LV ablation-induced HF rats displayed higher DPPIV activity in the plasma (≈50%) and heart tissue (≈3.5-fold) compared with sham-operated rats. Moreover, positive correlations were observed between the plasma DPPIV activity and LV end-diastolic pressure and lung congestion. Two days after surgery, 1 group of LV ablation-induced HF rats was treated with the DPPIV inhibitor sitagliptin (40 mg/kg BID) for 6 weeks, whereas the remaining rats were administered water. Hemodynamic measurements demonstrated that radiofrequency LV-ablated rats treated with sitagliptin exhibited a significant attenuation of HF-related cardiac dysfunction, including LV end-diastolic pressure, systolic performance, and chamber stiffness. Sitagliptin treatment also attenuated cardiac remodeling and cardiomyocyte apoptosis and minimized pulmonary congestion.Collectively, the results presented herein associate circulating DPPIV activity with poorer cardiovascular outcomes in human and experimental HF. Moreover, the results demonstrate that long-term DPPIV inhibition mitigates the development and progression of HF in rats.CONCLUSIONSCollectively, the results presented herein associate circulating DPPIV activity with poorer cardiovascular outcomes in human and experimental HF. Moreover, the results demonstrate that long-term DPPIV inhibition mitigates the development and progression of HF in rats. The present study addresses the hypothesis that the activity of dipeptidyl peptidase IV (DPPIV), an enzyme that inactivates peptides that possess cardioprotective actions, correlates with adverse outcomes in heart failure (HF). The therapeutic potential of DPPIV inhibition in preventing cardiac dysfunction is also investigated. Measurements of DPPIV activity in blood samples obtained from 190 patients with HF and 42 controls demonstrated that patients with HF exhibited an increase of ≈130% in circulating DPPIV activity compared with healthy subjects. Furthermore, an inverse correlation was observed between serum DPPIV activity and left ventricular (LV) ejection fraction in patients with HF. Similarly, radiofrequency LV ablation-induced HF rats displayed higher DPPIV activity in the plasma (≈50%) and heart tissue (≈3.5-fold) compared with sham-operated rats. Moreover, positive correlations were observed between the plasma DPPIV activity and LV end-diastolic pressure and lung congestion. Two days after surgery, 1 group of LV ablation-induced HF rats was treated with the DPPIV inhibitor sitagliptin (40 mg/kg BID) for 6 weeks, whereas the remaining rats were administered water. Hemodynamic measurements demonstrated that radiofrequency LV-ablated rats treated with sitagliptin exhibited a significant attenuation of HF-related cardiac dysfunction, including LV end-diastolic pressure, systolic performance, and chamber stiffness. Sitagliptin treatment also attenuated cardiac remodeling and cardiomyocyte apoptosis and minimized pulmonary congestion. Collectively, the results presented herein associate circulating DPPIV activity with poorer cardiovascular outcomes in human and experimental HF. Moreover, the results demonstrate that long-term DPPIV inhibition mitigates the development and progression of HF in rats. |
| Author | dos Santos, Leonardo Arruda-Junior, Daniel F. Mansur, Alfredo J. Antonio, Ednei L. Pereira, Alexandre C. Krieger, José E. Girardi, Adriana C.C. Campos, Luciene C.G. Tucci, Paulo J.F. Salles, Thiago A. Barreto, Ana Luiza T. |
| Author_xml | – sequence: 1 givenname: Leonardo surname: dos Santos fullname: dos Santos, Leonardo organization: From the Heart Institute (InCor), University of São Paulo Medical School, Brazil (L.d.S., T.A.S., D.F.A.-J., L.C.G.C., A.C.P., A.L.T.B., A.J.M., J.E.K., A.C.C.G.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil (L.d.S.); and Department of Physiology, Federal University of São Paulo University of São Paulo, Brazil (E.L.A., P.J.F.T.) – sequence: 2 givenname: Thiago A. surname: Salles fullname: Salles, Thiago A. organization: From the Heart Institute (InCor), University of São Paulo Medical School, Brazil (L.d.S., T.A.S., D.F.A.-J., L.C.G.C., A.C.P., A.L.T.B., A.J.M., J.E.K., A.C.C.G.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil (L.d.S.); and Department of Physiology, Federal University of São Paulo University of São Paulo, Brazil (E.L.A., P.J.F.T.) – sequence: 3 givenname: Daniel F. surname: Arruda-Junior fullname: Arruda-Junior, Daniel F. organization: From the Heart Institute (InCor), University of São Paulo Medical School, Brazil (L.d.S., T.A.S., D.F.A.-J., L.C.G.C., A.C.P., A.L.T.B., A.J.M., J.E.K., A.C.C.G.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil (L.d.S.); and Department of Physiology, Federal University of São Paulo University of São Paulo, Brazil (E.L.A., P.J.F.T.) – sequence: 4 givenname: Luciene C.G. surname: Campos fullname: Campos, Luciene C.G. organization: From the Heart Institute (InCor), University of São Paulo Medical School, Brazil (L.d.S., T.A.S., D.F.A.-J., L.C.G.C., A.C.P., A.L.T.B., A.J.M., J.E.K., A.C.C.G.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil (L.d.S.); and Department of Physiology, Federal University of São Paulo University of São Paulo, Brazil (E.L.A., P.J.F.T.) – sequence: 5 givenname: Alexandre C. surname: Pereira fullname: Pereira, Alexandre C. organization: From the Heart Institute (InCor), University of São Paulo Medical School, Brazil (L.d.S., T.A.S., D.F.A.-J., L.C.G.C., A.C.P., A.L.T.B., A.J.M., J.E.K., A.C.C.G.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil (L.d.S.); and Department of Physiology, Federal University of São Paulo University of São Paulo, Brazil (E.L.A., P.J.F.T.) – sequence: 6 givenname: Ana Luiza T. surname: Barreto fullname: Barreto, Ana Luiza T. organization: From the Heart Institute (InCor), University of São Paulo Medical School, Brazil (L.d.S., T.A.S., D.F.A.-J., L.C.G.C., A.C.P., A.L.T.B., A.J.M., J.E.K., A.C.C.G.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil (L.d.S.); and Department of Physiology, Federal University of São Paulo University of São Paulo, Brazil (E.L.A., P.J.F.T.) – sequence: 7 givenname: Ednei L. surname: Antonio fullname: Antonio, Ednei L. organization: From the Heart Institute (InCor), University of São Paulo Medical School, Brazil (L.d.S., T.A.S., D.F.A.-J., L.C.G.C., A.C.P., A.L.T.B., A.J.M., J.E.K., A.C.C.G.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil (L.d.S.); and Department of Physiology, Federal University of São Paulo University of São Paulo, Brazil (E.L.A., P.J.F.T.) – sequence: 8 givenname: Alfredo J. surname: Mansur fullname: Mansur, Alfredo J. organization: From the Heart Institute (InCor), University of São Paulo Medical School, Brazil (L.d.S., T.A.S., D.F.A.-J., L.C.G.C., A.C.P., A.L.T.B., A.J.M., J.E.K., A.C.C.G.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil (L.d.S.); and Department of Physiology, Federal University of São Paulo University of São Paulo, Brazil (E.L.A., P.J.F.T.) – sequence: 9 givenname: Paulo J.F. surname: Tucci fullname: Tucci, Paulo J.F. organization: From the Heart Institute (InCor), University of São Paulo Medical School, Brazil (L.d.S., T.A.S., D.F.A.-J., L.C.G.C., A.C.P., A.L.T.B., A.J.M., J.E.K., A.C.C.G.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil (L.d.S.); and Department of Physiology, Federal University of São Paulo University of São Paulo, Brazil (E.L.A., P.J.F.T.) – sequence: 10 givenname: José E. surname: Krieger fullname: Krieger, José E. organization: From the Heart Institute (InCor), University of São Paulo Medical School, Brazil (L.d.S., T.A.S., D.F.A.-J., L.C.G.C., A.C.P., A.L.T.B., A.J.M., J.E.K., A.C.C.G.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil (L.d.S.); and Department of Physiology, Federal University of São Paulo University of São Paulo, Brazil (E.L.A., P.J.F.T.) – sequence: 11 givenname: Adriana C.C. surname: Girardi fullname: Girardi, Adriana C.C. organization: From the Heart Institute (InCor), University of São Paulo Medical School, Brazil (L.d.S., T.A.S., D.F.A.-J., L.C.G.C., A.C.P., A.L.T.B., A.J.M., J.E.K., A.C.C.G.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil (L.d.S.); and Department of Physiology, Federal University of São Paulo University of São Paulo, Brazil (E.L.A., P.J.F.T.) |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23894014$$D View this record in MEDLINE/PubMed |
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| Snippet | The present study addresses the hypothesis that the activity of dipeptidyl peptidase IV (DPPIV), an enzyme that inactivates peptides that possess... |
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| SubjectTerms | Adult Aged Animals Apoptosis Biomarkers - blood Case-Control Studies Dipeptidyl Peptidase 4 - blood Dipeptidyl-Peptidase IV Inhibitors - pharmacology Disease Models, Animal Female Glucagon-Like Peptide 1 - blood Heart Failure - blood Heart Failure - drug therapy Heart Failure - enzymology Heart Failure - pathology Heart Failure - physiopathology Hemodynamics Humans Male Middle Aged Myocardium - enzymology Myocardium - pathology Natriuretic Peptide, Brain - blood Pulmonary Edema - enzymology Pulmonary Edema - prevention & control Pyrazines - pharmacology Rats Rats, Wistar Sitagliptin Phosphate Triazoles - pharmacology Up-Regulation Ventricular Function, Left Ventricular Remodeling |
| Title | Circulating Dipeptidyl Peptidase IV Activity Correlates With Cardiac Dysfunction in Human and Experimental Heart Failure |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/23894014 https://www.proquest.com/docview/1434022847 |
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