Preservation of glucose metabolism in hypertrophic GLUT4-null hearts

Antine E. Stenbit, Ellen B. Katz, John C. Chatham, David L. Geenen, Stephen M. Factor, Robert G. Weiss, Tsu Shuen Tsao, Ashwani Malhotra, V. P. Chacko, Christopher Ocampo, Linda A. Jelicks, Maureen J. Charron

Research output: Contribution to journalArticlepeer-review

39 Scopus citations


GLUT4-null mice lacking the insulin-sensitive glucose transporter are not diabetic but do exhibit abnormalities in glucose and lipid metabolism. The most striking morphological consequence of ablating GLUT4 is cardiac hypertrophy. GLUT4-null hearts display characteristics of hypertrophy caused by hypertension. However, GLUT4-null mice have normal blood pressure and maintain a normal cardiac contractile protein profile. Unexpectedly, although they lack the predominant glucose transporter in the heart, GLUT4-null hearts transport glucose and synthesize glycogen at normal levels, but gene expression of rate-limiting enzymes involved in fatty acid oxidation is decreased. The GLUT4-null heart represents a unique model of hypertrophy that may be used to study the consequences of altered substrate utilization in normal and pathophysiological conditions.

Original languageEnglish (US)
Pages (from-to)H313-H318
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number1 48-1
StatePublished - 2000


  • Glycogen
  • Nuclear magnetic resonance
  • Transport

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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