Skip Navigation

Cardiovascular Research 2001 52(3):407-416; doi:10.1016/S0008-6363(01)00393-5
© 2001 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Rosenblatt-Velin, N.
Right arrow Articles by Lerch, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rosenblatt-Velin, N.
Right arrow Articles by Lerch, R.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2001, European Society of Cardiology

Postinfarction heart failure in rats is associated with upregulation of GLUT-1 and downregulation of genes of fatty acid metabolism

Nathalie Rosenblatt-Velin, Christophe Montessuit, Irène Papageorgiou, Jérôme Terrand and René Lerch*

Cardiology Center, University Hospital, 24, rue Micheli-du-Crest CH-1211 Geneva 14, Switzerland

* Corresponding author. Tel.: +41-22-372-7202; fax: +41-22-372-7229 rene.lerch{at}hcuge.ch

Objectives: Increasing evidence suggests that left ventricular remodeling is associated with a shift from fatty acid to glucose metabolism for energy production. The aim of this study was to determine whether left ventricular remodeling with and without late-onset heart failure after myocardial infarction is associated with regional changes in the expression of regulatory proteins of glucose or fatty acid metabolism. Methods: Myocardial infarction was induced in rats by ligation of the left anterior descending coronary artery (LAD). In infarcted and sham-operated hearts the peri-infarction region (5-mm zone surrounding the region at risk), the interventricular septum and the right ventricular free wall were separated for analysis. Results: At 8 and 20 weeks after LAD ligation, the peri-infarction region and the septum exhibited marked re-expression of atrial natriuretic factor [+252±37 and +1093±279%, respectively, in the septum (P<0.05)] and of {alpha}-smooth muscle actin [+34±10 and +43±14%, respectively, in the septum (P<0.05)]. At 8 weeks, when left ventricular hypertrophy was present without signs of heart failure, myocardial mRNA expression of glucose transporters (GLUT-1 and GLUT-4) was not altered, whereas mRNA expression of medium-chain acyl-CoA dehydrogenase (MCAD) was significantly reduced in the peri-infarction region (–25±7%; P<0.05). In hearts exhibiting heart failure 20 weeks after infarct-induction there was a change in all three ventricular regions of both mRNA and protein content of GLUT-1 [+72±28 and +121±15%, respectively, in the peri-infarction region (P<0.05)] and MCAD [–29±9 and –56±4%, respectively, in the peri-infarction region (P<0.05)]. Conclusion: In rats with large myocardial infarction, progression from compensated remodeling to overt heart failure is associated with upregulation of GLUT-1 and downregulation of MCAD in both the peri-infarction region and the septum.

KEYWORDS Energy metabolism; Gene expression; Heart failure; Hypertrophy; Infarction; Remodeling


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
R. W. Schwenk, J. J.F.P. Luiken, A. Bonen, and J. F.C. Glatz
Regulation of sarcolemmal glucose and fatty acid transporters in cardiac disease
Cardiovasc Res, July 15, 2008; 79(2): 249 - 258.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.