Key result
Cardiac-specific expression of PPARβ/δ increased myocardial glucose utilization, prevented lipotoxic cardiomyopathy, and significantly reduced myocardial ischemia/reperfusion injury (infarct size 42.8% vs 59.9% in controls).
Why the study?
Does PPARbeta/delta activation improve myocardial glucose utilization and protect against ischemic injury and lipotoxic cardiomyopathy in mouse models?
Does PPARbeta/delta activation improve myocardial glucose utilization and protect against ischemic injury and lipotoxic cardiomyopathy in mouse models?
Absolute Event Rate: 42.8% vs 59.9%
p-value: p=<0.05
PPARbeta/delta activation drives a distinct metabolic program that increases myocardial glucose utilization and protects against ischemia/reperfusion injury without causing lipotoxic cardiomyopathy.
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Hypothesis-generating for PPARβ/δ-targeted metabolic therapy in cardiomyopathy; leaves open translation to human ischemia/reperfusion injury.
Burkart et al. (2007) studied Myocardial metabolism and ischemia/reperfusion injury. Cardiac-specific expression of PPARβ/δ (MHC-PPARβ/δ) vs. Non-transgenic (NTG) littermates and MHC-PPARα mice was evaluated on Myocardial ischemia/reperfusion injury (infarcted area relative to area at risk [IA/AAR]) (p=<0.05). Cardiac-specific expression of PPARβ/δ increased myocardial glucose utilization, prevented lipotoxic cardiomyopathy, and significantly reduced myocardial ischemia/reperfusion injury (infarct size 42.8% vs 59.9% in controls).
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