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Cardiovasc Res. 2015 May 1;106(2):194-205. doi: 10.1093/cvr/cvv105. Epub 2015 Mar 12.

Good and bad consequences of altered fatty acid metabolism in heart failure: evidence from mouse models.

Author information

1
Biomedical NMR, Department of Biomedical Engineering, Eindhoven University of Technology, High Tech Campus 11, 5656 AE, PO BOX 513, Eindhoven 5600 MB, The Netherlands.
2
Department of Genetics and Cell Biology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.
3
Biomedical NMR, Department of Biomedical Engineering, Eindhoven University of Technology, High Tech Campus 11, 5656 AE, PO BOX 513, Eindhoven 5600 MB, The Netherlands Department of Genetics and Cell Biology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands m.w.nabben@tue.nl m.nabben@maastrichtuniversity.nl.

Abstract

The shift in substrate preference away from fatty acid oxidation (FAO) towards increased glucose utilization in heart failure has long been interpreted as an oxygen-sparing mechanism. Inhibition of FAO has therefore evolved as an accepted approach to treat heart failure. However, recent data indicate that increased reliance on glucose might be detrimental rather than beneficial for the failing heart. This review discusses new insights into metabolic adaptations in heart failure. A particular focus lies on data obtained from mouse models with modulations of cardiac FA metabolism at different levels of the FA metabolic pathway and how these differently affect cardiac function. Based on studies in which these mouse models were exposed to ischaemic and non-ischaemic heart failure, we discuss whether and when modulations in FA metabolism are protective against heart failure.

KEYWORDS:

Energy metabolism; Genetically altered mice; Heart failure; Metabolic shift

PMID:
25765936
DOI:
10.1093/cvr/cvv105
[Indexed for MEDLINE]

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