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October 4, 2005CirculationOpen Access

Decreased Contractile and Metabolic Reserve in Peroxisome Proliferator–Activated Receptor-α–Null Hearts Can Be Rescued by Increasing Glucose Transport and Utilization

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Key result

Overexpressing the glucose transporter GLUT1 in PPARalpha-null mouse hearts corrected metabolic and functional defects during high workload challenge.

Why the study?

Does overexpressing GLUT1 improve contractile and metabolic reserve in PPARalpha-null hearts?

Population

Perfused hearts isolated from genetically modified mice (PPARalpha) that mimic the metabolic profile in…

Comparison

Overexpressing the insulin-independent glucose… vs PPARalpha(-/-) hearts without GLUT1 overexpression

Design

Preclinical

Authors

ILIvan LuptakBoston UniversityJBJames A. BalschiBoston UniversityYXYanqiu XingQilu Hospital of Shandong University

Discussion

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Implication

Supports GLUT1 as metabolic target in hypertrophy models; leaves open clinical translation to human heart failure.

Structured PICO

Does overexpressing GLUT1 improve contractile and metabolic reserve in PPARalpha-null hearts?

P
Population
Perfused hearts isolated from genetically modified mice (PPARalpha(-/-)) that mimic the metabolic profile in myocardial hypertrophy
I
Intervention
Overexpressing the insulin-independent glucose transporter GLUT1
C
Comparator
PPARalpha(-/-) hearts without GLUT1 overexpression
O
Outcome
Contractile function, substrate utilization, and high-energy phosphate metabolism (ATP synthesis) during high workload challengesurrogate

Enhancing myocardial glucose utilization via GLUT1 overexpression rescues contractile and metabolic reserve in PPARalpha-deficient hearts, suggesting a potential therapeutic strategy for pathological hypertrophy.

Cite This Study

Luptak et al. (2005) studied Myocardial hypertrophy / PPARalpha deficiency. Overexpressing the insulin-independent glucose transporter GLUT1 vs. PPARalpha(-/-) hearts without GLUT1 overexpression was evaluated on Contractile function and high-energy phosphate metabolism during high workload challenge. Overexpressing the glucose transporter GLUT1 in PPARalpha-null mouse hearts corrected metabolic and functional defects during high workload challenge.

synapsesocial.com/papers/6a178aa08d470cd99253615chttps://doi.org/10.1161/circulationaha.105.534594
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Also Consider

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

  1. 1Contribution of oxidative metabolism and glycolysis to ATP production in hypertrophied hearts1994 · 580 citations
  2. 2Reaction rates of creatine kinase and ATP synthesis in the isolated rat heart. A 31P NMR magnetization transfer study.1985 · 291 citations
  3. 3Synthesis, transfer, and phosphorylation of phosphoinositides in cardiac membranes1990 · 180 citations
  4. 4Reactivation of Peroxisome Proliferator-activated Receptor α Is Associated with Contractile Dysfunction in Hypertrophied Rat Heart2001 · 255 citations
  5. 5Mechanisms for Increased Glycolysis in the Hypertrophied Rat Heart2004 · 245 citations