Preservation of glucose metabolism in hypertrophic GLUT4-null hearts.

Academic Article


  • 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.
  • Keywords

  • Animals, Blood Pressure, Cardiomegaly, Deoxyglucose, Diastole, Female, Glucose, Glucose Transporter Type 4, Hypertension, Magnetic Resonance Imaging, Male, Mice, Mice, Knockout, Monosaccharide Transport Proteins, Muscle Proteins, Myocardium, Sex Characteristics
  • Digital Object Identifier (doi)

    Author List

  • Stenbit AE; Katz EB; Chatham JC; Geenen DL; Factor SM; Weiss RG; Tsao TS; Malhotra A; Chacko VP; Ocampo C
  • Start Page

  • H313
  • End Page

  • H318
  • Volume

  • 279
  • Issue

  • 1