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Articles in PresS, published online ahead of print April 30, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00072.2002
Submitted on February 19, 2002
Accepted on April 22, 2002
1 Cardiovascular Research Institute, Morehouse School of Medicine, Atlanta, GA, USA; Medicine, Lillehei Heart Institute, University of Minnesota, Minneapolis, MN, USA
2 Cardiovascular Research Institute, Morehouse School of Medicine, Atlanta, GA, USA
3 Center for NMR Research and Development, University of Alabama at Birmingham, Birmingham, AL, USA
* To whom correspondence should be addressed. E-mail: hallx068{at}umn.edu.
13C-NMR spectroscopy was used to test our hypothesis that insulin-like growth factor I (IGF-I) stimulates glucose flux into both non-oxidative and oxidative pathways in vascular smooth muscle cells (VSMC). Rat VSMC were exposed to uniformly labeled 13C-glucose ([U-13C]6-glucose)(5.5 mM) and [3-13C]pyruvate (1 mM) in the presence and absence of IGF-I (100 ng/ml). IGF-1 increased glucose flux through glycolysis and the TCA cycle as well as total anaplerotic flux into the TCA cycle. Previous work in our lab identified an increase in GLUT1 content and glucose metabolism in neointimal VSMC that was sufficient to promote proliferation and inhibit apoptosis. To test if IGF-I could potentiate the GLUT-1-induced increased flux in the neointima, we utilized VSMC harboring constitutive overexpression of GLUT1. Indeed, IGF-I markedly potentiated the GLUT1-induced increase in glucose flux through glycolysis and the TCA cycle. Taken together, these findings demonstrate that up-regulation of glucose transport through either IGF-I or increased GLUT1 content stimulates glucose flux through both non-oxidative and oxidative pathways in VSMC.
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