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.
Park
James L
JL
Internal Medicine, Division of Nephrology, University of Michigan Medical School, 1560 MSRB 2, 1150 W. Medical Center Drive, Ann Arbor, MI 48109-0676, USA.
Heilig
Charles W
CW
Brosius
Frank C
FC
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