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Angiotensin-converting enzyme inhibition and food restriction in diabetic mice do not correct the increased sensitivity for ischemia-reperfusion injury

DOI: 10.1186/1475-2840-11-89

Keywords: Ischemia/reperfusion, Diabetes mellitus, Metabolic syndrome, In vivo contractility, Infarct size

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Abstract:

C57Bl6/J wild type (WT) mice, leptin deficient ob/ob (model for type II diabetes) and double knock-out (LDLR-/-;ob/ob, further called DKO) mice with combined leptin and LDL-receptor deficiency (model for metabolic syndrome) were used. The effects of 12?weeks food restriction or ACE-I on infarct size and load-independent left ventricular contractility after 30?min regional cardiac ischemia were investigated. Differences between groups were analyzed for statistical significance by Student’s?t-test or factorial ANOVA followed by a Fisher’s LSD post hoc test.Infarct size was larger in ob/ob and DKO versus WT. Twelve weeks of ACE-I improved pre-ischemic left ventricular contractility in ob/ob and DKO. Twelve weeks of food restriction, with a weight reduction of 35-40%, or ACE-I did not reduce the effect of IR.ACE-I and food restriction do not correct the increased sensitivity for cardiac IR-injury in mouse models of type II diabetes and the metabolic syndrome.The number of patients with diabetes and the metabolic syndrome increases in Western societies and reaches epidemic proportions [1,2]. At present, diabetes affects approximately 250 million people worldwide and by 2025 this is expected to increase to over 380 million, with type II diabetes accounting for 90-95% of them. Prevalence is expected to increase most in Asia and Africa with the majority of patients in 2030 being found there [2]. The prevalence of the metabolic syndrome currently exceeds 20% of individuals who are over 20?years of age and 40% of the population older than 40?years [1]. Heart failure is the leading cause of mortality in people with type II diabetes. The incidence of myocardial infarction in diabetic patients is twice that of the general population [3,4]. They are at increased risk for mortality and post-ischemic complications [3,4]. Infarct size for a given ischemic insult is larger in diabetic mice than in controls [5-7]. This, on top of diabetic cardiomyopathy [8,9], contributes to progressi

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