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Am J Physiol Endocrinol Metab 282: E1039-E1045, 2002. First published January 29, 2002; doi:10.1152/ajpendo.00507.2001
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Vol. 282, Issue 5, E1039-E1045, May 2002

Accelerated rates of glycolysis in the hypertrophied heart: are they a methodological artifact?

Hon Sing Leong1, Mark Grist1, Hannah Parsons1, Richard B. Wambolt1, Gary D. Lopaschuk3, Roger Brownsey2, and Michael F. Allard1

1 McDonald Research Laboratories/The iCAPTUR4 E Centre, Department of Pathology and Laboratory Medicine, University of British Columbia-St. Paul's Hospital, Vancouver, British Columbia, V6Z 1Y6; 2 Department of Biochemistry and Molecular Biology, University of British Columbia, Vancouver, V6T 1Z3; and 3 Cardiovascular Research Group, University of Alberta, Edmonton, Alberta, Canada T6G 2S2

Glycolysis, measured by 3H2O production from [5-3H]glucose, is accelerated in isolated working hypertrophied rat hearts. However, nonglycolytic detritiation of [5-3H]glucose via the nonoxidative pentose phosphate pathway (PPP) could potentially lead to an overestimation of true glycolytic rates, especially in hypertrophied hearts where the PPP may be upregulated. To address this concern, we measured glycolysis using [5-3H]glucose and a second, independent method in isolated working hearts from halothane-anesthetized, sham-operated and aortic-constricted rats. Glycolysis was accelerated in hypertrophied hearts compared with control hearts regardless of the method used. There was also excellent concordance in glycolytic rates between the different methods. Moreover, activity of glucose-6-phosphate dehydrogenase and expression of transaldolase, enzymes controlling key steps in the oxidative and nonoxidative PPP, respectively, were not different between control and hypertrophied hearts. Thus nonglycolytic detritiation of [5-3H]glucose in the PPP is insignificant, and 3H2O production from [5-3H]glucose is an accurate means to measure glycolysis in isolated working normal and hypertrophied rat hearts. Furthermore, the PPP does not appear to be increased in cardiac hypertrophy induced by abdominal aortic constriction.

pentose phosphate pathway; glucose-6-phosphate dehydrogenase; transaldolase


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