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Objectives Insulin exerts significant cardioprotective effects in acute myocardial ischaemia/reperfusion (MI/R) through the PI3K-Akt signalling. The present study was aimed at investigating the effect of insulin treatment on the prolonged postischemic cardiac structural and functional changes. Methods Adult male rats were subjected to left anterior descending coronary artery occlusion and were randomised to receive one of the following treatments: saline, early insulin treatment or late insulin treatment (the same dose and routine of insulin starting at 1 week after the surgery). Results Infarct size was significantly reduced in early but not late insulin treatment group compared to control group 4 wks after MI (30.2±2.5% vs 45.2±2.6%, n=6, p Conclusion These data indicate that early but not late insulin treatment improves left ventricular remodelling and cardiac function in rat MI model, myocardial insulin resistance may be one possible mechanism that abolished the cardioprotective effects of late insulin treatment on cardiac structure and function.

Introduction Switched myocardial substrate uptake from fatty acids to carbohydrate has been proposed to resist ischemia/reperfusion injury. We hypothesised that altered myocardial substrate uptake during early reperfusion may contribute to IPC-afforded cardioprotection. Methods Adult male rats were subjected to 30 min of myocardial ischemia and 3 h of reperfusion (MI/R). IPC was achieved by two cycles of 5 min ischemia and 5 min reperfusion. Myocardial glucose and fatty acid (FA) uptake were assessed at the end of 1 h reperfusion by determining fluorodeoxyglucose uptake and fatty acid translocase (FAT)/CD36 translocation, respectively. Results IPC significantly improved cardiac functions, reduced myocardial infarction, apoptotic cell death and blood CK/LDH levels following MI/R (all p Conclusions IPC increased both glucose and FA uptake during early reperfusion to resist myocardial injury via insulin/PI3K-dependent Akt and AMPK activation. Therefore, augmenting insulin signaling may be a potential therapy to improve myocardial substrate uptake and restore the cardioprotection of IPC in the diabetic hearts.