Document Detail


Normalizing the metabolic phenotype after myocardial infarction: impact of subchronic high fat feeding.
MedLine Citation:
PMID:  22542451     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The normal heart relies primarily on the oxidation of fatty acids (FA) for ATP production, whereas during heart failure (HF) glucose utilization increases, implying pathological changes to cardiac energy metabolism. Despite the noted lipotoxic effects of elevating FA, our work has demonstrated a cardioprotective effect of a high fat diet (SAT) when fed after myocardial infarction (MI), as compared to normal chow (NC) fed cohorts. This data has suggested a mechanistic link to energy metabolism. The goal of this study was to determine the impact of SAT on the metabolic phenotype of the heart after MI. Male Wistar rats underwent coronary ligation surgery (MI) and were evaluated after 8 weeks of SAT. Induction of MI was verified by echocardiography. LV function assessed by in vivo hemodynamic measurements revealed improvements in the MI-SAT group as compared to MI-NC. Perfused working hearts revealed a decrease in cardiac work in MI-NC that was improved in MI-SAT. Glucose oxidation was increased and FA oxidation decreased in MI-NC compared to shams suggesting an alteration in the metabolic profile that was ameliorated by SAT. (31)P NMR analysis of Langendorff perfused hearts revealed no differences in PCr:ATP indicating no overt energy deficit in MI groups. Phospho-PDH and PDK(4) were increased in MI-SAT, consistent with a shift towards fatty acid oxidation (FAO). Overall, these results support the hypothesis that SAT post-infarction promotes a normal metabolic phenotype that may serve a cardioprotective role in the injured heart.
Authors:
Jessica M Berthiaume; Martin E Young; Xiaoqin Chen; Tracy A McElfresh; Xin Yu; Margaret P Chandler
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-04-20
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  53     ISSN:  1095-8584     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-06-11     Completed Date:  2012-10-19     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  125-33     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Ltd. All rights reserved.
Affiliation:
Dept of Physiology & Biophysics, Case Western Reserve University, 10900 Euclid Ave., Cleveland, OH 44106-4970, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism
Animals
Diet, High-Fat*
Disease Models, Animal
Echocardiography
Energy Metabolism
Hemodynamics
Male
Metabolome*
Myocardial Infarction / metabolism*,  physiopathology
Myocardium / metabolism
Phenotype
Phosphocreatine / metabolism
Phosphorylation
Protein Kinases / metabolism
Pyruvate Dehydrogenase Complex / metabolism
Rats
Grant Support
ID/Acronym/Agency:
HL081857/HL/NHLBI NIH HHS; R01 HL081857/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Pyruvate Dehydrogenase Complex; 56-65-5/Adenosine Triphosphate; 67-07-2/Phosphocreatine; EC 2.7.-/Protein Kinases; EC 2.7.1.-/pyruvate dehydrogenase kinase 4
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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