title: Metabolic and molecular consequences of modifying GLUT4 expression in skeletal muscle.
abstract: We have described mouse models in which the expression levels of GLUT4 in skeletal muscle have been modified. GLUT4 null mice, which lack skeletal-muscle GLUT4, are insulin-resistant. In contrast, MLC-GLUT4 mice, which overexpress GLUT4 specifically in the skeletal muscle, exhibit an increase in insulin-sensitivity and glucose disposal. Restoring GLUT4 expression specifically in the skeletal muscle of the GLUT4 null mice by mating with MLC-GLUT4 transgenic mice normalizes the reduced glucose uptake and glucose metabolism of the skeletal muscle of the MLC-GLUT4 null mouse. These models represent unique agents to dissect the mechanism for insulin signalling and GLUT4 translocation in skeletal muscle that expresses varying levels of GLUT4.
authors.affiliation: Department of Biochemistry, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
authors.forename: M J
authors.initials: MJ
authors.lastname: Charron
authors.forename: E B
authors.initials: EB
authors.lastname: Katz
authors.forename: J R
authors.initials: JR
authors.lastname: Zierath
mesh_terms: D000818:Animals; D005947:Glucose / Q000378:metabolism; D051272:Glucose Transporter Type 1; D051275:Glucose Transporter Type 4; D007328:Insulin / Q000494:pharmacology; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D009004:Monosaccharide Transport Proteins / Q000096:biosynthesis* / Q000172:deficiency*; D009124:Muscle Proteins; D018482:Muscle, Skeletal / Q000187:drug effects / Q000502:physiology*; D011994:Recombinant Proteins / Q000096:biosynthesis; D015398:Signal Transduction
chemical_list: D051272:Glucose Transporter Type 1; D051275:Glucose Transporter Type 4; D007328:Insulin; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; D011994:Recombinant Proteins; C495693:Slc2a4 protein, mouse; D005947:Glucose