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High Glucose Alters Cardiomyocyte Contacts and Inhibits Myofibrillar Formation

Divisions of Endocrinology and Diabetes (D.D., M.Y.D.) and Nephrology (J.K., P.A.), University Hospital, CH-8091 Zurich, Switzerland; and Institute of Pharmacology and Toxicology (P.S., M.C.S.), University of Zurich, CH-8032 Zurich, Switzerland

Address all correspondence and requests for reprints to: Marc Y. Donath, M.D., Division of Endocrinology and Diabetes, University Hospital of Zurich, Rämistrasse 100, CH-8091 Zurich, Switzerland. E-mail: marc.donath{at}usz.ch.

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 -actin were reduced, whereas the nonsarcomeric smooth muscle -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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