Abstract
Compared to the lean Lou/C rat, the Wistar rat develops increased body weight 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 electron flux and inducing significantly increased cardio-toxicity. Inhibitors of respiratory complex II could thus help protect the heart against ischemia/reperfusion in obese individuals.
Highlights
Obesity exacerbates the incidence of coronary heart disease [1] but seems to have a contradictory effect on cardiac susceptibility to ischemic damage (CSI)
This study aimed to determine whether increased abdominal adiposity (IAA) during the early phase of systemic glucose intolerance due to augmented intake of a low-fat diet equilibrated in lipids, can alter the recovery of mechanical function during post-ischemic reperfusion
Their body weights and densities were higher compared to Lou/C rats (323 ± 5 vs. 188 ± 11 g, +72%, p
Summary
Obesity exacerbates the incidence of coronary heart disease [1] but seems to have a contradictory effect on cardiac susceptibility to ischemic damage (CSI). With SCM, CSI decreases [2,3] whereas, with HF diets, similar to so-called Western diets rich in saturated fats, CSI increases [4,5,6,7,8,9]. Both peri-natal over-nutrition (ON) and genetically modified rodents with a hyperphagic behaviour have been found to have increased calorie intake, but when allowed to eat a normal diet, ON rodents have increased CSI [10,11,12]. The diabetic Zucker fatty rat, a genetic model of hyperphagy and hyperglycaemia caused by a Westerntype diet, displays decreased CSI until the age of 6 months [13,14] but has increased CSI thereafter [15]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
