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Updated: Aug 12, 2026

Methods for the Determination of Rates of Glucose and Fatty Acid Oxidation in the Isolated Working Rat Heart
Published on: September 28, 2016
Glycolysis and pyruvate oxidation in cardiac hypertrophy--why so unbalanced?
H S Leong1, R W Brownsey, J E Kulpa
1McDonald Research Laboratories/The iCAPTUR4E Centre, Department of Pathology and Laboratory Medicine, University of British Columbia, St. Paul's Hospital, 1081 Burrard Street, Vancouver, BC, Canada V6Z 1Y6.
Insights
Cardiac hypertrophy alters heart energy metabolism, uncoupling glucose use and production. Impaired pyruvate dehydrogenase complex (PDC) function is not the sole cause, suggesting other metabolic pathways are involved.
Area of Science:
- Biochemistry
- Cardiology
- Metabolic research
Background:
- Cardiac hypertrophy involves abnormal heart energy metabolism and structural changes.
- Increased glycolysis and glucose utilization occur, but pyruvate oxidation doesn't match pyruvate production.
- This leads to uncoupled glycolysis and glucose oxidation in hypertrophied hearts.
Purpose of the Study:
- To test the hypothesis that pyruvate dehydrogenase complex (PDC) function is impaired in cardiac hypertrophy.
- To investigate the mechanisms behind altered pyruvate metabolism in hypertrophied hearts.
Main Methods:
- Review of existing evidence on cardiac hypertrophy and glucose metabolism.
- Analysis of the role of pyruvate dehydrogenase complex (PDC) in controlling glucose oxidation.
- Discussion of potential alternative mechanisms affecting pyruvate metabolism.
Main Results:
- Alterations in glucose metabolism in cardiac hypertrophy are not solely explained by changes in PDC expression or control.
- Evidence suggests that altered pyruvate metabolism involves more than just PDC function.
Conclusions:
- The uncoupling of glycolysis and glucose oxidation in cardiac hypertrophy is complex.
- Additional factors, including pyruvate transport, NADH shuttles, lactate dehydrogenase, and amino acid metabolism, may contribute to altered pyruvate metabolism.
Abstract:
Cardiac hypertrophy, induced by chronic pressure or volume overload, is associated with abnormalities in energy metabolism as well as characteristic increases in muscle mass and alterations in the structure of the heart. Hypertrophied hearts display increased rates of glycolysis and overall glucose utilization, but rates of pyruvate oxidation do not rise in step with rates of pyruvate generation. Glycolysis and glucose oxidation, therefore, become markedly less 'coupled' in hypertrophied hearts than in non-hypertrophied hearts. Because the pyruvate dehydrogenase complex (PDC) contributes so powerfully to the control of glucose oxidation, we set out to test the hypothesis that the function of PDC is impaired in cardiac hypertrophy. In this review we describe evidence indicating that the alterations in glucose metabolism in hypertrophied hearts cannot be explained simply by changes in PDC expression or control. Additional mechanisms that may lead to an altered balance of pyruvate metabolism in cardiac hypertrophy are discussed, with commentaries on possible changes in pyruvate transport, NADH shuttles, lactate dehydrogenase, and amino acid metabolism.
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