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

Michael F. Allard, Richard B. Wambolt, Sarah L. Longnus, Mark Grist, Carmen P. Lydell, Hannah L. Parsons, Brian Rodrigues, Jennifer L. Hall, William C. Stanley, Gregory P. Bondy

Research output: Contribution to journalArticlepeer-review

46 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)E487-E493
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume279
Issue number3 42-3
DOIs
StatePublished - 2000

Keywords

  • Cardiac hypertrophy
  • Glucose oxidation
  • Glycogen
  • Glycolysis
  • Insulin resistance

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