Document Detail

Chronic and acute exposure of mouse hearts to fatty acids increases oxygen cost of excitation-contraction coupling.
MedLine Citation:
PMID:  21335471     Owner:  NLM     Status:  Publisher    
The aim of the present study was to evaluate the underlying processes involved in the oxygen wasting induced by inotropic drugs and acute and chronic elevation of fatty acid (FA) supply, using unloaded perfused mouse hearts from normal and type 2 diabetic (db/db) mice. We found that an acute elevation of the FA supply in normal hearts, as well as a chronic (in vivo) exposure to elevated FA as of in db/db hearts, increased MVO(2unloaded) due to increased oxygen cost for basal metabolism (BM) and for excitation-contraction (E-C) coupling. Isoproterenol stimulation, on top of a high FA supply led to an additive increase in MVO(2unloaded), due to a further increase in oxygen cost for E-C coupling. In db/db hearts, acute elevation of FA did not further increase MVO(2). Since elevation in the FA supply is accompanied by increased rates of myocardial FA oxidation, the present study compared MVO(2) following increased FA load versus FA oxidation rate by exposing normal hearts to normal and high FA concentration (NF and HF), and to compounds that either stimulate (GW610742) or inhibit (dichloroacetate, DCA) FA oxidation. While HF and NF+GW increased FA oxidation to the same extent, only HF increased MVO(2unloaded). Although DCA counteracted the HF-induced increase in FA oxidation, DCA did not reduce MVO(2unloaded). Thus, in normal hearts, acute FA-induced oxygen waste is i) due to an increase in the oxygen cost for both basal metabolism and E-C coupling, and ii) not dependent on the myocardial FA oxidation rate per se, but on processes initiated by the presence of FAs. In diabetic hearts, chronic exposure to elevated circulating FAs leads to adaptations that afford protection against the detrimental effect of an acute FA load, suggesting different underlying mechanisms behind the increased MVO(2) following acute and chronic FA load.
Neoma T Boardman; Terje S Larsen; David L Severson; M Faadiel Essop; Ellen Aasum
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-2-18
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  -     ISSN:  1522-1539     ISO Abbreviation:  -     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-2-21     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
1University of Tromsoe Faculty of Health Sciences.
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