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July 29, 2006AJP Heart and Circulatory Physiology

Role of the α2-isoform of AMP-activated protein kinase in the metabolic response of the heart to no-flow ischemia

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Key result

AMPKalpha(2) deletion in mice resulted in a more rapid onset of ischemia-induced contracture and decreased ATP and glycogen content, but did not exacerbate impairment of postischemic contractile recovery.

Why the study?

Does AMPKalpha2 deletion alter the metabolic response and contractile function of the heart during no-flow ischemia in mice?

Population

AMPKalpha2-knockout (AMPKalpha2(-/-)) mice and wild-type mice

Comparison

AMPKalpha2 deletion subjected to no-flow ischemia vs Wild-type mice subjected to no-flow ischemia

Design

Preclinical

Authors

EZElham ZarrinpashnehKing's College LondonKCKarla CarjavalCBChristophe BeauloyeInterventional Cardiology

Discussion

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Implication

Metabolic deficits from AMPKα2 deletion do not worsen postischemic recovery in mice; leaves open translational relevance.

Key Points

  • This study aims to investigate the specific role of AMPKalpha(2) in the heart's metabolic response during ischemia.
  • Used AMPKalpha(2)-knockout mice to assess metabolic responses during normoxia and ischemia with glucose substrate
  • Conducted hemodynamic measurements via echocardiography
  • Evaluated ATP content, lactate production, glycogen content, and phosphorylation state of acetyl-CoA carboxylase.
  • Hearts from AMPKalpha(2)(-/-) mice showed a rapid onset of ischemia-induced contracture compared to wild-type
  • AMPKalpha(2)(-/-) mice exhibited decreased ATP content, lactate production, glycogen content, and AMPKbeta(2) content during ischemia
  • Despite metabolic impairments during ischemia, AMPKalpha(2) absence did not worsen postischemic contractile recovery.

Structured PICO

Does AMPKalpha2 deletion alter the metabolic response and contractile function of the heart during no-flow ischemia in mice?

P
Population
AMPKalpha(2)-knockout mice evaluated for the consequences of AMPKalpha(2) deletion during normoxia and ischemia.
E
Exposure
AMPKalpha2 deletion (knockout model) subjected to no-flow ischemia
C
Comparator
Wild-type mice subjected to no-flow ischemia
O
Outcome
Metabolic response and contractile function during normoxia and no-flow ischemia (including onset of ischemia-induced contracture, ATP content, lactate production, glycogen content, and postischemic contractile function recovery)surrogate

AMPKalpha2 is required for the metabolic response of the heart to no-flow ischemia, and its absence leads to worse metabolic adaptation but does not worsen postischemic contractile recovery.

Cite This Study

Zarrinpashneh et al. (2006) studied No-flow ischemia. AMPKalpha(2) deletion vs. Wild-type animals was evaluated on Metabolic response and contractile function during normoxia and ischemia. AMPKalpha(2) deletion in mice resulted in a more rapid onset of ischemia-induced contracture and decreased ATP and glycogen content, but did not exacerbate impairment of postischemic contractile recovery.

synapsesocial.com/papers/6a6bf0a7ff619b1ab2cb39e6https://doi.org/10.1152/ajpheart.01032.2005
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Also Consider

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

  1. 1Translocation of myocardial GLUT-4 and increased glucose uptake through activation of AMPK by AICAR1999 · 550 citations
  2. 2Rate of glycolysis during ischemia determines extent of ischemic injury and functional recovery after reperfusion1994 · 113 citations
  3. 3AMP-activated protein kinase: greater AMP dependence, and preferential nuclear localization, of complexes containing the α2 isoform1998 · 439 citations
  4. 4Insulin antagonizes AMP‐activated protein kinase activation by ischemia or anoxia in rat hearts, without affecting total adenine nucleotides2001 · 122 citations
  5. 5Glycogen debranching enzyme association with β-subunit regulates AMP-activated protein kinase activity2005 · 36 citations