Postexercise glucose uptake and glycogen synthesis in skeletal muscle from GLUT4-deficient mice.
To determine the role of GLUT4 on postexercise glucose transport and glycogen resynthesis in skeletal muscle, GLUT4-deficient and wild-type mice were studied after a 3 h swim exercise. In wild-type mice, insulin and swimming each increased 2-deoxyglucose uptake by twofold in extensor digitorum longus muscle. In contrast, insulin did not increase 2-deoxyglucose glucose uptake in muscle from GLUT4-null mice. Swimming increased glucose transport twofold in muscle from fed GLUT4-null mice, with no effect noted in fasted GLUT4-null mice. This exercise-associated 2-deoxyglucose glucose uptake was not accompanied by increased cell surface GLUT1 content. Glucose transport in GLUT4-null muscle was increased 1.6-fold over basal levels after electrical stimulation. Contraction-induced glucose transport activity was fourfold greater in wild-type vs. GLUT4-null muscle. Glycogen content in gastrocnemius muscle was similar between wild-type and GLUT4-null mice and was reduced approximately 50% after exercise. After 5 h carbohydrate refeeding, muscle glycogen content was fully restored in wild-type, with no change in GLUT4-null mice. After 24 h carbohydrate refeeding, muscle glycogen in GLUT4-null mice was restored to fed levels. In conclusion, GLUT4 is the major transporter responsible for exercise-induced glucose transport. Also, postexercise glycogen resynthesis in muscle was greatly delayed; unlike wild-type mice, glycogen supercompensation was not found. GLUT4 it is not essential for glycogen repletion since muscle glycogen levels in previously exercised GLUT4-null mice were totally restored after 24 h carbohydrate refeeding.-Ryder, J. W., Kawano, Y., Galuska, D., Fahlman, R., Wallberg-Henriksson, H., Charron, M. J., Zierath, J. R. Postexercise glucose uptake and glycogen synthesis in skeletal muscle from GLUT4-deficient mice.
Ryder
J W
JW
Department of Clinical Physiology, Karolinska Hospital, S-171 76, Department of Physiology and Pharmacology, Karolinska Institute, S-171 77, Stockholm, Sweden.
Kawano
Y
Y
Galuska
D
D
Fahlman
R
R
Wallberg-Henriksson
H
H
Charron
M J
MJ
Zierath
J R
JR
D000818:Animals; D001692:Biological Transport; D001786:Blood Glucose / Q000378:metabolism; D004040:Dietary Carbohydrates; D005215:Fasting; D005947:Glucose / Q000378:metabolism*; D051272:Glucose Transporter Type 1; D051275:Glucose Transporter Type 4; D006003:Glycogen / Q000096:biosynthesis* / Q000378:metabolism; D006006:Glycogen Synthase / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009004:Monosaccharide Transport Proteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D009119:Muscle Contraction / Q000502:physiology; D009124:Muscle Proteins; D018482:Muscle, Skeletal / Q000378:metabolism*; D005082:Physical Exertion
D001786:Blood Glucose; D004040:Dietary Carbohydrates; D051272:Glucose Transporter Type 1; D051275:Glucose Transporter Type 4; D008565:Membrane Proteins; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; C495678:Slc2a1 protein, mouse; C495693:Slc2a4 protein, mouse; D006003:Glycogen; D006006:Glycogen Synthase; D005947:Glucose