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Articles in PresS, published online ahead of print May 23, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00275.2002
Submitted on March 28, 2002
Accepted on May 22, 2002
1 Pediatrics, University of Alberta, Edmonton, Alberta, Canada; Pharmacology, University of Alberta, Edmonton, Alberta, Canada
2 Pharmacology, University of Alberta, Edmonton, Alberta, Canada
3 Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: jason.dyck{at}ualberta.ca.
In this study isolated perfused working rat hearts were used to investigate the role of palmitate-regulated PKB phosphorylation on glucose metabolism. Rat hearts were perfused aerobically in working mode with 11 mM glucose, and either 100 µU/ml insulin or 100 µU/ml insulin and 1.2 mM palmitate. PKB activity and phosphorylation state were reduced in the presence of 1.2 mM palmitate, which correlates with a decrease in glycolysis (47%), glucose oxidation (84%), and glucose uptake (43%). In contrast to skeletal muscle, neither p38 nor ERK underwent changes in their phosphorylation states in response to insulin or insulin and palmitate. Moreover, pharmacological restoration of glucose oxidation rates in hearts perfused with 1.2 mM palmitate demonstrated no increase in PKB phosphorylation state. In cultured mouse cardiac muscle HL-1 cells, insulin markedly increased PKB phosphorylation, which was blunted by pre- and co-treatment with 1.2 mM palmitate. However, neither palmitate nor C2-ceramide treatment of insulin-stimulated cells was able to accelerate PKB dephosphorylation beyond that observed following the removal of insulin alone. Taken together, these experiments show the control of PKB phosphorylation by palmitate is independent of ceramide and suggest that this signaling event may be an important regulator of myocardial glucose uptake and oxidation.
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