| Literature DB >> 25765936 |
Desiree Abdurrachim1, Joost J F P Luiken2, Klaas Nicolay1, Jan F C Glatz2, Jeanine J Prompers1, Miranda Nabben3.
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. Published on behalf of the European Society of Cardiology. All rights reserved.Entities:
Keywords: Energy metabolism; Genetically altered mice; Heart failure; Metabolic shift
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Year: 2015 PMID： 25765936 DOI： 10.1093/cvr/cvv105
Source DB: PubMed Journal: Cardiovasc Res ISSN： 0008-6363 Impact factor: 10.787