PERSISTENT MYOCARDIAL-ISCHEMIA INCREASES GLUT1 GLUCOSE-TRANSPORTER EXPRESSION IN BOTH ISCHEMIC AND NON ISCHEMIC HEART REGIONS

Citation
Fc. Brosius et al., PERSISTENT MYOCARDIAL-ISCHEMIA INCREASES GLUT1 GLUCOSE-TRANSPORTER EXPRESSION IN BOTH ISCHEMIC AND NON ISCHEMIC HEART REGIONS, Journal of Molecular and Cellular Cardiology, 29(6), 1997, pp. 1675-1685
Citations number
42
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
00222828
Volume
29
Issue
6
Year of publication
1997
Pages
1675 - 1685
Database
ISI
SICI code
0022-2828(1997)29:6<1675:PMIGGE>2.0.ZU;2-U
Abstract
Persistently ischemic myocardium exhibits increased glucose uptake whi ch may contribute to the preservation of myocardial function and viabi lity. Little is known about the specific molecular events which are re sponsible for this increase in uptake. Therefore, we investigated whet her myocardial ischemia induces the gene expression of the major cardi ac facilitative glucose transporters, GLUT4 and GLUT1. We determined t he expression of myocardial glucose transporter mRNAs and polypeptides after 6 h of regional ischemia in a dog model by semi-quantitative No rthern blotting and immunoblotting. GLUT1 but not GLUT4 expression was significantly increased in both ischemic and non-ischemic regions fro m the experimental hearts when compared to surgical control and normal hearts. GLUT1 mRNA expression was increased 3.4-fold and GLUT1 polype ptide expression was increased 1.7-fold in ischemic hearts when compar ed to normal or surgical-control hearts. There were no significant reg ional differences in GLUT1 expression in either normal or ischemic hea rts. However, there was a tendency for GLUT1 mRNA expression to be hig hest in the non-ischemic regions from the 6-h ischemia hearts. These f indings suggest that myocardial ischemia induces a factor or factors w hich stimulate GLUT1 expression in non-ischemic as well as ischemic my ocardial regions. Increased GLUT1 expression may play a role in augmen ting glucose uptake during ischemia. (C) 1997 Academic Press Limited.