Increased Abdominal Adiposity Exacerbates Ex-Vivo Cardiac Reperfusion Injury through Augmented Mitochondrial Oxidative StressDamien Vitiello1,4*, Evangelia Mourmoura1,2, Karine Couturier1,2, Patrick Faure5, Herve Dubouchaud1,2, Corinne Malpuech-Brugere6, Kasra Azarnoush6,7 and Luc Demaison1,2,6
- *Corresponding Author:
- D. Vitiello
Institut de Recherche biomédicale et d’Épidemiologie du Sport (IRMES)
Institut National du Sport de l’Expertise et de la Performance (INSEP)
Paris, France. Université Paris Descartes,
Sorbonne Paris Cité, EA 7329, Paris, France
E-mail: [email protected]
Received date: September 21, 2015; Accepted date: October 08, 2015; Published date: October 12, 2015
Citation: Vitiello D, Mourmoura E, Couturier K, Faure P, Dubouchaud H, et al. (2015) Increased Abdominal Adiposity Exacerbates Ex-Vivo Cardiac Reperfusion Injury through Augmented Mitochondrial Oxidative Stress. J Diabetes Metab 6:614. doi: 10.4172/2155-6156.1000614
Copyright: © 2015 Vitiello D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Compared to the lean Lou/C rat, the Wistar rat develops increased
and abdominal adiposity (IAA). The aim of this study was to compare the functional response to cardiac ischemia/reperfusion of 3-month old Wistar rats with age-matched Lou/C rats, and to explain the differences with regards to mitochondrial hydrogen-peroxide release (mH2O2r). Langendorff-perfused hearts of Lou/C and Wistar rats were subjected to ischemia (25 min) followed by reperfusion (30 min). Cardiac function was monitored throughout the experiment. Mitochondria were extracted before and after ischemia, and their oxidative capacities, mH2O2r, and activity of the respiratory-chain complex were measured. The IAA of Wistar rats was associated with slight glucose intolerance and noticeable functional abnormalities of the myocardium during post-ischemic reperfusion. Cardio-toxicity was related to maintenance of the activity of respiratory-chain complex II and increased mH2O2r, whereas cardio-protection in lean Lou/C rats occurred through reduced complex-II activity and mH2O2r. In conclusion, IAA and/or systemic glucose intolerance maintained complex-II activity during post-ischemic reperfusion, thus increasing mH2O2r through reverse
flux and inducing significantly increased cardio-toxicity.
of respiratory complex II could thus help protect the heart against ischemia/reperfusion in obese individuals.