Abstract
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.
Publication types
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Comparative Study
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Acetylcholine / pharmacology
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Animals
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Aorta, Thoracic / drug effects
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Aorta, Thoracic / metabolism
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Dose-Response Relationship, Drug
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Endothelium, Vascular / drug effects
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Endothelium, Vascular / metabolism*
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Glucose Transporter Type 1
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In Vitro Techniques
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Mice
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Mice, Transgenic
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Monosaccharide Transport Proteins / biosynthesis
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Monosaccharide Transport Proteins / deficiency*
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Monosaccharide Transport Proteins / genetics
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Vasodilation / drug effects
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Vasodilation / physiology*
Substances
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Glucose Transporter Type 1
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Monosaccharide Transport Proteins
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Slc2a1 protein, mouse
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Acetylcholine