GLUT1-deficient mice exhibit impaired endothelium-dependent vascular relaxation.
We tested the hypothesis that decreased glucose transporter 1 (GLUT1) expression alters endothelial function. Nitric oxide-dependent endothelial relaxation, but not endothelium-independent relaxation, was significantly reduced in aortas from transgenic mice expressing GLUT1 antisense mRNA, compared to aortas from nontransgenic littermates. These data suggest that GLUT1-dependent glucose metabolism may play an important role in regulating endothelial function.
Internal Medicine, Division of Nephrology, University of Michigan Medical School, 1560 MSRB 2, 1150 W. Medical Center Drive, Ann Arbor, MI 48109-0676, USA.
James L
JL
Park
Charles W
CW
Heilig
Frank C
FC
Brosius
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism*; D051272:Glucose Transporter Type 1; D066298:In Vitro Techniques; D051379:Mice; D008822:Mice, Transgenic; D009004:Monosaccharide Transport Proteins / Q000096:biosynthesis / Q000172:deficiency* / Q000235:genetics; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
D051272:Glucose Transporter Type 1; D009004:Monosaccharide Transport Proteins; C495678:Slc2a1 protein, mouse; D000109:Acetylcholine