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1 Université Paris-Sud, Inserm U-769; IFR-141, Chatenay-Malabry, France
2 Division of Cardiology, School of Medicine Université Catholique de Louvain, Brussels, Belgium
3 Chatenay-Malabry, France; Université Paris-Sud, Inserm U-769; IFR-141, Chatenay-Malabry, France
4 RMN biologique, ICSN, Gif-sur-Yvette, France
5 Université René Descartes, U-567 Inserm; UMR 8104 CNRS; Institut Cochin, Paris, France
6 Paris, France; Université René Descartes, U-567 Inserm; UMR 8104 CNRS; Institut Cochin, France
7 Département des Facteurs humains, CRSSA, La Tronche, France
8 Brussels, Belgium; Division of Cardiology, School of Medicine Université Catholique de Louvain, Brussels, Belgium
* To whom correspondence should be addressed. E-mail: jacqueline.hoerter{at}cep.u-psud.fr.
IBecause the question "is 
2-AMPK isoform a friend or a foe in the protection of the myocardium against ischemia-reperfusion injury?"is still in debate, we studied the functional consequence of its deletion on the contractility, the energetics, and the respiration of the isolated perfused heart and characterized the response to low flow ischemia and reperfusion with glucose and pyruvate as substrates. Alpha2 deletion did not affect basal contractility, respiration and high energy phosphate contents but induced a 2 fold reduction in glycogen content and a 3 fold reduction in glucose uptake. Low flow ischemia (LFI) increased AMPK phosphorylation and stimulated glucose uptake and phosphorylation in both 2-KO and WT. The high sensitivity of 2-KO to the development of ischemic contracture was attributed to the constitutive impairment in glucose transport and glycogen content and not a perturbation of the energy transfer by creatine kinase (CK). The functional coupling of MM-CK to myofibrillar ATPase and the CK fluxes were indeed similar in 2-KO and WT. LFI impaired CK flux by 50% in both strains, showing that 2-AMPK does not control CK activity. Despite the higher sensitivity to contracture, the post ischemic contractility recovered to similar level in both 2-KO and WT in the absence of fatty acids . In their presence, 2-AMPK deletion also accelerated the contracture, but delayed post-ischemic contractile recovery. In conclusion 2-AMPK is required for a normal glucose uptake and glycogen content which protects the heart from the development of the ischemic contracture, but not for contractile recovery in the absence of fatty acids.
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