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January 1, 2012Frontiers in PhysiologyOpen Access

5′-AMP Activated Protein Kinase is Involved in the Regulation of Myocardial β-Oxidative Capacity in Mice

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Population

Young and old mice expressing a dominant negative AMPKα2 construct and their wildtype littermates

Comparison

Expression of a dominant negative AMPKα2 construct vs Wildtype (WT) littermates

Design

Preclinical

Authors

NSNis StrideSLSteen LarsenJTJonas T. Treebak

Discussion

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Overview

Does not yet inform clinical cardiac energetics; leaves open AMPK modulation effects on human MCFA oxidation.

Structured PICO

P
Population
Young and old mice expressing a dominant negative AMPKα2 (AMPKα2-KD) construct and their wildtype (WT) littermates
I
Intervention
Expression of a dominant negative AMPKα2 (AMPKα2-KD) construct
C
Comparator
Wildtype (WT) littermates
O
Outcome
Mitochondrial oxidative phosphorylation capacity from the oxidation of long- and medium-chain fatty acids (LCFA and MCFA) in cardiomyocytessurrogate

AMPK is necessary for normal mitochondrial function in the heart, and its decreased activity reduces the capacity to oxidize medium-chain fatty acids, potentially altering the energetic state.

Cite This Study

Stride et al. (2012) studied this question.

synapsesocial.com/papers/6a7044aafebe604dd7090c42https://doi.org/10.3389/fphys.2012.00033
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Role of the α<sub>2</sub>-isoform of AMP-activated protein kinase in the metabolic response of the heart to no-flow ischemia2006 · 92 citations
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  4. 4AMPK activation increases uncoupling protein-3 expression and mitochondrial enzyme activities in rat muscle without fibre type transitions2003 · 100 citations
  5. 5Moderate severity heart failure does not involve a downregulation of myocardial fatty acid oxidation2004 · 134 citations