Key result
Streptozotocin-induced diabetes led to a 3.3-fold increase in cardiac cell apoptosis (0.0069% vs 0.0021%, P<0.001) and reduced cardiomyocyte contacts, while high glucose in vitro inhibited myofibrillar formation.
A diabetic milieu induces structural alterations in the heart, including apoptosis, loss of intercellular contacts, and malformation of contractile structures, which can be prevented by antioxidants.
CONTEXT: The frequency of diabetes-related heart failure along with the prevalence of diabetes is increasing. Diabetic cardiomyopathy is considered to be a distinct disease in the absence of discernible coronary artery and other defined heart disease. Previously we have shown that glucose and palmitic acid induce degeneration of myofibrils and modulate apoptosis in cultivated cardiomyocytes. OBJECTIVE: Here we studied the mechanisms of diabetic cardiomyopathy in more detail. RESULTS: Streptozotocin-induced diabetes led to a significant increase in cardiac cell apoptosis. Furthermore, cardiomyocyte contacts were reduced. In vitro, prolonged exposure of cultured adult cardiomyocytes to high glucose concentrations drastically reduced myofibrillar formation. In particular, sarcomeric myosin heavy chains and cardiac alpha-actin were reduced, whereas the nonsarcomeric smooth muscle alpha-actin remained unaffected. The deleterious effects of glucose on myofibril formation were prevented by antioxidative regimens. CONCLUSIONS: Thus, a diabetic milieu leads to multiple structural alterations of the heart including apoptosis, loss of intercellular contacts, and malformation of contractile structures.
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Dyntar et al. (2006) studied Diabetic cardiomyopathy (n=10). Streptozotocin-induced diabetes and high glucose exposure vs. Buffer injection (in vivo); 5.5 mmol/liter glucose (in vitro) was evaluated on Cardiac cell apoptosis (TUNEL-positive nuclei) (3.3-fold increase, p=<0.001). Streptozotocin-induced diabetes led to a 3.3-fold increase in cardiac cell apoptosis (0.0069% vs 0.0021%, P<0.001) and reduced cardiomyocyte contacts, while high glucose in vitro inhibited myofibrillar formation.
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