Document Detail


Pressure-overload induced heart failure induces a selective reduction in glucose oxidation at physiological afterload.
MedLine Citation:
PMID:  23257023     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
AIMS: Development of heart failure is known to be associated with changes in energy substrate metabolism. Information on the changes in energy substrate metabolism that occur in heart failure is limited and results vary depending on the methods employed. Our aim is to characterize the changes in energy substrate metabolism associated with pressure overload and ischemia-reperfusion injury.Methods and ResultsWe used transverse aortic constriction (TAC) in mice to induce pressure overload-induced heart failure. Metabolic rates were measured in isolated working hearts perfused at physiological afterload (80 mmHg) using (3)H or (14)C labeled substrates. As a result of pressure-overload injury, murine hearts exhibited: (1) hypertrophy, systolic and diastolic dysfunctions; (2) reduction in LV work, (3) reduced rates of glucose and lactate oxidations, with no change in glycolysis or fatty acid oxidation and a small decrease in triacylglycerol oxidation, and (4) increased phosphorylation of AMPK and a reduction in malonyl-CoA levels. Sham hearts produced more acetyl CoA from carbohydrates than from fats, whereas TAC hearts showed a reverse trend. Ischemia-reperfusion (I/R) in sham group produced a metabolic switch analogous to the TAC-induced shift to fatty acid oxidation, whereas I/R in TAC hearts greatly exacerbated the existing imbalance, and was associated with a poorer recovery during reperfusion. CONCLUSIONS: Pressure overload-induced heart failure and I/R shift the preference of substrate oxidation from glucose and lactate to fatty acid due to a selective reduction in carbohydrate oxidation. Normalizing the balance between metabolic substrate utilization may alleviate pressure-overload induced heart failure and ischemia.
Authors:
Pavel Zhabyeyev; Manoj Gandhi; Jun Mori; Ratnadeep Basu; Zamaneh Kassiri; Alexander Clanachan; Gary D Lopaschuk; Gavin Y Oudit
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-12-19
Journal Detail:
Title:  Cardiovascular research     Volume:  -     ISSN:  1755-3245     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-12-21     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Division of Cardiology, Department of Medicine, University of Alberta, Edmonton, Canada.
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