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Am J Physiol Endocrinol Metab 279: E487-E493, 2000;
0193-1849/00 $5.00
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Vol. 279, Issue 3, E487-E493, September 2000

Hypertrophied rat hearts are less responsive to the metabolic and functional effects of insulin

Michael F. Allard1, Richard B. Wambolt1, Sarah L. Longnus1, Mark Grist1, Carmen P. Lydell1, Hannah L. Parsons1, Brian Rodrigues2, Jennifer L. Hall3, William C. Stanley4, and Gregory P. Bondy1

1 Cardiovascular Research Laboratory, Department of Pathology and Laboratory Medicine, University of British Columbia-St. Paul's Hospital, Vancouver, British Columbia V6Z 1Y6; 2 Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3; 3 Cardiovascular Research Institute, Morehouse Medical School, Atlanta, Georgia, 30310; and 4 Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106-4970

We determined the effect of insulin on the fate of glucose and contractile function in isolated working hypertrophied hearts from rats with an aortic constriction (n = 27) and control hearts from sham-operated rats (n = 27). Insulin increased glycolysis and glycogen in control and hypertrophied hearts. The change in glycogen was brought about by increased glycogen synthesis and decreased glycogenolysis in both groups. However, the magnitude of change in glycolysis, glycogen synthesis, and glycogenolysis caused by insulin was lower in hypertrophied hearts than in control hearts. Insulin also increased glucose oxidation and contractile function in control hearts but not in hypertrophied hearts. Protein content of glucose transporters, protein kinase B, and phosphatidylinositol 3-kinase was not different between the two groups. Thus hypertrophied hearts are less responsive to the metabolic and functional effects of insulin. The reduced responsiveness involves multiple aspects of glucose metabolism, including glycolysis, glucose oxidation, and glycogen metabolism. The absence of changes in content of key regulatory molecules indicates that other sites, pathways, or factors regulating glucose utilization are responsible for these findings.

cardiac hypertrophy; insulin resistance; glycolysis; glucose oxidation; glycogen


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