Autophagy contributes to retardation of cardiac growth in diabetic rats
2012
Lee, Y.J., Graduate School of Inje University, Gimhae, Republic of Korea | Hong, Y.K., Graduate School of Inje University, Gimhae, Republic of Korea | Lee, S.R., National Primate Research Center, KRIBB, Ochang, Republic of Korea | Chang, K.T., National Primate Research Center, KRIBB, Ochang, Republic of Korea | Hong, Y.G., Graduate School of Inje University, Gimhae, Republic of Korea
Diabetes mellitus is a major predictor of heart failure, although the mechanisms by which the disease causes cardiomyopathy are not well understood. The purpose of this study was to determine whether prolonged exposure of cardiomyocytes to high glucose concentrations induces autophagy and contributes to cardiomyopathy. Interestingly, there were no differences in the autophagic activation produced by different glucose concentrations. However, cell viability was decreased by high glucose. In the diabetic rats, we found a higher level of microtubule-associated protein light chain 3 (LC3) expression and a reduction in the size of the left ventricle (LV) (P less than 0.05) caused by growth retardation, suggesting activated autophagy. Our in vitro findings indicate that hyperglycemic oxidative stress induces autophagy, and our in vivo studies reveal that autophagy is involved in the progression of pathophysiological remodeling of the heart. Taken together, the studies suggest that autophagy may play a role in the pathogenesis of juvenile diabetic cardiomyopathy.
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