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Am J Physiol Heart Circ Physiol (April 28, 2006). doi:10.1152/ajpheart.01147.2005
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Submitted on October 31, 2005
Accepted on April 18, 2006

EFFECTS OF ADENOSINE ON MYOCARDIAL GLUCOSE AND PALMITATE METABOLISM AFTER TRANSIENT ISCHEMIA: ROLE OF 5'-AMP-ACTIVATED PROTEIN KINASE

Jagdip S Jaswal1, Manoj Gandhi1, Barry A Finegan1, Jason R Dyck1, and Alexander S Clanachan1*

1 Pharmacology, University of Alberta, Edmonton, Canada

* To whom correspondence should be addressed. E-mail: sclanachan{at}pmcol.ualberta.ca.

The loss of cardioprotection by adenosine in hearts stressed by transient ischemia may be due to its effects on glucose metabolism. In the absence of transient ischemia, adenosine inhibits glycolysis, while it accelerates glycolysis following transient ischemia. As 5'-AMP-activated protein kinase (AMPK) is implicated as a regulator of glucose and fatty acid utilization, this study determined whether a differential alteration of AMPK activity contributes to the acceleration of glycolysis by adenosine in hearts stressed by transient ischemia. Studies were performed in working rat hearts perfused aerobically under normal conditions or following transient ischemia (2x10 min ischemia followed by 5 min reperfusion). LV work was not affected by adenosine. AMPK phosphorylation was not affected by transient ischemia per se, however, phosphorylation and activity were increased 9- and 3-fold, respectively by adenosine in stressed hearts. The phosphorylation of acetyl-CoA carboxylase and rates of palmitate oxidation were unaltered. Glycolysis and calculated proton production were increased 1.8- and 1.7-fold respectively in hearts with elevated AMPK activity. Elevated AMPK activity was associated with inhibition of glycogen synthesis and unchanged rates of glucose uptake and glycogenolysis. Phentolamine, an {alpha}-adrenoceptor antagonist, which prevents adenosine-induced activation of glycolysis in stressed hearts prevented AMPK phosphorylation. These data demonstrate that adenosine-induced activation of AMPK following transient ischemia is not sufficient to alter palmitate oxidation or glucose uptake. Rather, activation of AMPK alters the partitioning of glucose away from glycogen synthesis thereby increasing glycolysis that may in part contribute to the loss of adenosine-induced cardioprotection in hearts subjected to transient ischemia.




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