Abstract:
:Patients with left ventricle (LV) volume overload (VO) remain in a compensated state for many years although severe dilation is present. The myocardial capacity to fulfill its energetic demand may delay decompensation. We performed a gene expression profile, a model of chronic VO in rat LV with severe aortic valve regurgitation (AR) for 9 months, and focused on the study of genes associated with myocardial energetics. Methods. LV gene expression profile was performed in rats after 9 months of AR and compared to sham-operated controls. LV glucose and fatty acid (FA) uptake was also evaluated in vivo by positron emission tomography in 8-week AR rats treated or not with fenofibrate, an activator of FA oxidation (FAO). Results. Many LV genes associated with mitochondrial function and metabolism were downregulated in AR rats. FA β-oxidation capacity was significantly impaired as early as two weeks after AR. Treatment with fenofibrate, a PPARα agonist, normalized both FA and glucose uptake while reducing LV dilation caused by AR. Conclusion. Myocardial energy substrate preference is affected early in the evolution of LV-VO cardiomyopathy. Maintaining a relatively normal FA utilization in the myocardium could translate into less glucose uptake and possibly lesser LV remodeling.
journal_name
Biomed Res Intjournal_title
BioMed research internationalauthors
Roussel E,Drolet MC,Walsh-Wilkinson E,Dhahri W,Lachance D,Gascon S,Sarrhini O,Rousseau JA,Lecomte R,Couet J,Arsenault Mdoi
10.1155/2015/949624subject
Has Abstractpub_date
2015-01-01 00:00:00pages
949624eissn
2314-6133issn
2314-6141journal_volume
2015pub_type
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journal_title:BioMed research international
pub_type: 杂志文章
doi:10.1155/2013/971096
更新日期:2013-01-01 00:00:00
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