| First Author | Stenbit AE | Year | 2000 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 279 |
| Issue | 1 | Pages | H313-8 |
| PubMed ID | 10899071 | Mgi Jnum | J:107849 |
| Mgi Id | MGI:3622378 | Doi | 10.1152/ajpheart.2000.279.1.H313 |
| Citation | Stenbit AE, et al. (2000) Preservation of glucose metabolism in hypertrophic GLUT4-null hearts. Am J Physiol Heart Circ Physiol 279(1):H313-8 |
| abstractText | 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. |
