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Articles in PresS, published online ahead of print January 29, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00507.2001
Submitted on November 12, 2001
Accepted on January 23, 2002
1 Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada
2 Cardiovascular Research Group, University of Alberta, Edmonton, Alberta, Canada
3 Biochemistry and Molecular Biology, Univeristy of British Columbia, Vancouver, British Columbia, Canada
* To whom correspondence should be addressed. E-mail: mallard{at}mrl.ubc.ca.
Glycolysis, measured by 3H2O production from [5-3H]-glucose, is accelerated in isolated working hypertrophied rat hearts. However, non-glycolytic detritiation of [5-3H]-glucose via the non-oxidative 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 to control hearts, regardless of method used. There was also excellent concordance in glycolytic rates between the different methods. Moreover, glucose-6-phosphate dehydrogenase activity and transaldolase expression, enzymes controlling key steps in the oxidative and non-oxidative PPP, respectively, were not different between control and hypertrophied hearts. Thus, non-glycolytic 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.
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