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Am J Physiol Heart Circ Physiol 279: H313-H318, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 1, H313-H318, July 2000

Preservation of glucose metabolism in hypertrophic GLUT4-null hearts

Antine E. Stenbit1,*, Ellen B. Katz1,*, John C. Chatham2, David L. Geenen3,4, Stephen M. Factor3,5, Robert G. Weiss6, Tsu-Shuen Tsao1, Ashwani Malhotra7, V. P. Chacko2, Christopher Ocampo6, Linda A. Jelicks4, and Maureen J. Charron1

Departments of 1 Biochemistry, 3 Medicine, 4 Physiology and Biophysics, and 5 Pathology, Albert Einstein College of Medicine, Bronx, New York 10461-1602; 2 Division of NMR Research, Department of Radiology, and 6 Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205-2195; and 7 Division of Nephrology, Department of Medicine, University of Medicine and Dentistry at New Jersey, Newark, New Jersey 07103

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.

transport; glycogen; nuclear magnetic resonance

*  A. E. Stenbit and E. B. Katz contributed equally to this work.




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