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The accelerated post‐infarction progression of cardiac remodelling is associated with genetic changes in an untreated streptozotocin‐induced diabetic rat model
Author(s) -
Song GuangYuan,
Wu YongJian,
Yang YueJin,
Li JianJun,
Zhang HongLiang,
Pei HanJun,
Zhao ZhenYan,
Zeng ZengHua,
Hui RuTai
Publication year - 2009
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1093/eurjhf/hfp117
Subject(s) - medicine , streptozotocin , diabetes mellitus , heart failure , cardiology , myocardial infarction , endocrinology
Aims The mechanism by which diabetes mellitus exacerbates myocardial injury and the incidence of heart failure after acute myocardial infarction (AMI), remains unclear. We studied the severity of cardiac dysfunction and time‐dependent gene expression in a hyperglycaemic rat model with AMI. Methods and results The diabetic model was produced by injection of streptozotocin in Sprague‐Dawley rats. Ten weeks after induction of diabetes, AMI was induced by ligation of the left anterior descending coronary artery. Cardiac function and left ventricular (LV) dimensions were evaluated using two‐dimensional echocardiography. Structural changes were assessed by histological examination. Gene expression profile was documented by using affymetrix genechip U230 2.0 array and real time‐PCR. During 56 days post‐AMI, lower survival rates, worse LV function, more severe fibrosis, and larger LV diameters were identified in diabetic rats compared with non‐diabetic rats. A total 1221 genes involved in processes, such as glucose metabolism, fatty acid metabolism, extracellular matrix, and apoptosis, were found to be differentially expressed between diabetic and non‐diabetic rats, of these 770 were up‐regulated and 451 down‐regulated. Up‐regulation of the genes was found 1–2 weeks earlier in diabetic rats than in non‐diabetic rats. Conclusion The present data suggest that hyperglycaemia up‐regulates remodelling‐related genes, which may be responsible for the worse outcomes in diabetics than in non‐diabetics after AMI.