Document Detail

High glucose alters cardiomyocyte contacts and inhibits myofibrillar formation.
MedLine Citation:
PMID:  16522700     Owner:  NLM     Status:  MEDLINE    
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.
Daniela Dyntar; Pavel Sergeev; Jelena Klisic; Patrice Ambühl; Marcus C Schaub; Marc Y Donath
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-03-07
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  91     ISSN:  0021-972X     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2006 May 
Date Detail:
Created Date:  2006-05-08     Completed Date:  2006-06-07     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1961-7     Citation Subset:  AIM; IM    
Division of Endocrinology and Diabetes, University Hospital of Zurich, Rämistrasse 100, CH-8091 Zurich, Switzerland.
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MeSH Terms
Antioxidants / pharmacology
Apoptosis / drug effects
Blotting, Western
Cell Communication / drug effects
Cell Size
Cells, Cultured
Deoxyglucose / metabolism
Diabetes Mellitus, Experimental / pathology*
Glucose / metabolism,  pharmacology*
Heart Ventricles / cytology,  drug effects
Myocytes, Cardiac / drug effects,  pathology*,  ultrastructure
Myofibrils / drug effects,  pathology*,  ultrastructure
Organ Size / drug effects
Oxidative Stress / drug effects
Reg. No./Substance:
0/Antioxidants; 154-17-6/Deoxyglucose; 50-99-7/Glucose

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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