DPP-4 inhibitor and estrogen share similar efficacy against cardiac ischemic-reperfusion injury in obese-insulin resistant and estrogen-deprived female rats

© The Author(s) 2017. Estrogen deprivation aggravates cardiac injury after myocardial ischemia and reperfusion (I/R) injury. Although either estrogen or the dipeptidyl peptidase-4 (DPP-4) inhibitor, vildagliptin, reduces myocardial damage following cardiac I/R, their effects on the heart in obese-in...

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Main Authors: Sivaporn Sivasinprasasn, Pongpan Tanajak, Wanpitak Pongkan, Wasana Pratchayasakul, Siriporn C. Chattipakorn, Nipon Chattipakorn
Format: Journal
Published: 2018
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http://cmuir.cmu.ac.th/jspui/handle/6653943832/57983
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spelling th-cmuir.6653943832-579832018-09-05T03:55:48Z DPP-4 inhibitor and estrogen share similar efficacy against cardiac ischemic-reperfusion injury in obese-insulin resistant and estrogen-deprived female rats Sivaporn Sivasinprasasn Pongpan Tanajak Wanpitak Pongkan Wasana Pratchayasakul Siriporn C. Chattipakorn Nipon Chattipakorn Multidisciplinary © The Author(s) 2017. Estrogen deprivation aggravates cardiac injury after myocardial ischemia and reperfusion (I/R) injury. Although either estrogen or the dipeptidyl peptidase-4 (DPP-4) inhibitor, vildagliptin, reduces myocardial damage following cardiac I/R, their effects on the heart in obese-insulin resistant and estrogen deprived conditions remain unknown. Ovariectomized (O) rats (n = 36) were divided to receive either normal diet (NDO) or high-fat diet (HFO) for 12 weeks, followed by treatment with a vehicle, estrogen or vildagliptin for 4 weeks. The setting of in vivo cardiac I/R injury, 30-min ischemia and 120-min reperfusion, was performed. At 12 weeks after ovariectomy, both NDO and HFO rats exhibited an obese-insulin resistant condition. Both NDO and HFO rats treated with estrogen and vildagliptin showed reduced fasting plasma glucose, insulin and HOMA index. Both treatments improved cardiac function indicated by restoration of heart rate variability and increased %left ventricular ejection fraction (%LVEF). The treatments similarly protected cardiac mitochondrial function against I/R injury, leading to a reduction in the infarct size, oxidative stress and apoptosis in the ischemic myocardium. These findings demonstrate that vildagliptin effectively improves metabolic status, and shares similar efficacy to estrogen in reducing myocardial infarction and protecting cardiac mitochondrial function against I/R injury in estrogen-deprived obese-insulin resistant rats. 2018-09-05T03:55:48Z 2018-09-05T03:55:48Z 2017-03-10 Journal 20452322 2-s2.0-85014942592 10.1038/srep44306 https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85014942592&origin=inward http://cmuir.cmu.ac.th/jspui/handle/6653943832/57983
institution Chiang Mai University
building Chiang Mai University Library
country Thailand
collection CMU Intellectual Repository
topic Multidisciplinary
spellingShingle Multidisciplinary
Sivaporn Sivasinprasasn
Pongpan Tanajak
Wanpitak Pongkan
Wasana Pratchayasakul
Siriporn C. Chattipakorn
Nipon Chattipakorn
DPP-4 inhibitor and estrogen share similar efficacy against cardiac ischemic-reperfusion injury in obese-insulin resistant and estrogen-deprived female rats
description © The Author(s) 2017. Estrogen deprivation aggravates cardiac injury after myocardial ischemia and reperfusion (I/R) injury. Although either estrogen or the dipeptidyl peptidase-4 (DPP-4) inhibitor, vildagliptin, reduces myocardial damage following cardiac I/R, their effects on the heart in obese-insulin resistant and estrogen deprived conditions remain unknown. Ovariectomized (O) rats (n = 36) were divided to receive either normal diet (NDO) or high-fat diet (HFO) for 12 weeks, followed by treatment with a vehicle, estrogen or vildagliptin for 4 weeks. The setting of in vivo cardiac I/R injury, 30-min ischemia and 120-min reperfusion, was performed. At 12 weeks after ovariectomy, both NDO and HFO rats exhibited an obese-insulin resistant condition. Both NDO and HFO rats treated with estrogen and vildagliptin showed reduced fasting plasma glucose, insulin and HOMA index. Both treatments improved cardiac function indicated by restoration of heart rate variability and increased %left ventricular ejection fraction (%LVEF). The treatments similarly protected cardiac mitochondrial function against I/R injury, leading to a reduction in the infarct size, oxidative stress and apoptosis in the ischemic myocardium. These findings demonstrate that vildagliptin effectively improves metabolic status, and shares similar efficacy to estrogen in reducing myocardial infarction and protecting cardiac mitochondrial function against I/R injury in estrogen-deprived obese-insulin resistant rats.
format Journal
author Sivaporn Sivasinprasasn
Pongpan Tanajak
Wanpitak Pongkan
Wasana Pratchayasakul
Siriporn C. Chattipakorn
Nipon Chattipakorn
author_facet Sivaporn Sivasinprasasn
Pongpan Tanajak
Wanpitak Pongkan
Wasana Pratchayasakul
Siriporn C. Chattipakorn
Nipon Chattipakorn
author_sort Sivaporn Sivasinprasasn
title DPP-4 inhibitor and estrogen share similar efficacy against cardiac ischemic-reperfusion injury in obese-insulin resistant and estrogen-deprived female rats
title_short DPP-4 inhibitor and estrogen share similar efficacy against cardiac ischemic-reperfusion injury in obese-insulin resistant and estrogen-deprived female rats
title_full DPP-4 inhibitor and estrogen share similar efficacy against cardiac ischemic-reperfusion injury in obese-insulin resistant and estrogen-deprived female rats
title_fullStr DPP-4 inhibitor and estrogen share similar efficacy against cardiac ischemic-reperfusion injury in obese-insulin resistant and estrogen-deprived female rats
title_full_unstemmed DPP-4 inhibitor and estrogen share similar efficacy against cardiac ischemic-reperfusion injury in obese-insulin resistant and estrogen-deprived female rats
title_sort dpp-4 inhibitor and estrogen share similar efficacy against cardiac ischemic-reperfusion injury in obese-insulin resistant and estrogen-deprived female rats
publishDate 2018
url https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85014942592&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/57983
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