Preservation of glucose metabolism in hypertrophic GLUT4-null hearts

Academic Article

Abstract

  • 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.
  • Author List

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

  • 279
  • Issue

  • 1 48-1