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Restoration of glucose metabolism in leptin-resistant model hearts after acute myocardial infarction through the activation of survival kinase pathways

Witham W et al. – These data demonstrate that impaired cardiac leptin signaling results in metabolic inflexibility for glucose utilization in the face of cardiac stress, and greater morbidity after MI. Further, these studies show that cardiac glucose metabolism can be restored in leptin–resistant hearts by CNTF–mediated activation of survival kinases, resulting in multiple improved structural and functional outcomes post–MI. [more...]

Journal of Molecular and Cellular Cardiology

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