Metabolic and molecular consequences of modifying GLUT4 expression in skeletal muscle.
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.
Charron
M J
MJ
Department of Biochemistry, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Katz
E B
EB
Zierath
J R
JR
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
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