Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/50939
Título: GLUT4 and glycogen synthase are key players in bed rest-induced insulin resistance
Autores/as: Biensø, Rasmus S.
Ringholm, Stine
Kiilerich, Kristian
Aachmann-Andersen, Niels Jacob
Krogh-Madsen, Rikke
Guerra, Borja 
Plomgaard, Peter
Van Hall, Gerrit
Treebak, Jonas T.
Saltin, Bengt
Lundby, Carsten
Calbet, Jose A. L. 
Pilegaard, Henriette
Wojtaszewski, Jørgen F.P.
Clasificación UNESCO: 241106 Fisiología del ejercicio
Palabras clave: Human Skeletal-Muscle
Exercise-Induced Increase
Glucose-Uptake
Stimulated Phosphorylation
Gene-Expression, et al.
Fecha de publicación: 2012
Editor/a: 0012-1797
Publicación seriada: Diabetes (New York, N.Y.) 
Resumen: To elucidate the molecular mechanisms behind physical inactivity– induced insulin resistance in skeletal muscle, 12 young, healthy male subjects completed 7 days of bed rest with vastus lateralis muscle biopsies obtained before and after. In six of the subjects, muscle biopsies were taken from both legs before and after a 3-h hyperinsulinemic euglycemic clamp performed 3 h after a 45-min, one-legged exercise. Blood samples were obtained from one femoral artery and both femoral veins before and during the clamp. Glucose infusion rate and leg glucose extraction during the clamp were lower after than before bed rest. This bed rest–induced insulin resistance occurred together with reduced muscle GLUT4, hexokinase II, protein kinase B/Akt1, and Akt2 protein level, and a tendency for reduced 3-hydroxyacyl-CoA dehydrogenase activity. The ability of insulin to phosphorylate Akt and activate glycogen synthase (GS) was reduced with normal GS site 3 but abnormal GS site 2+2a phosphorylation after bed rest. Exercise enhanced insulin-stimulated leg glucose extraction both before and after bed rest, which was accompanied by higher GS activity in the prior-exercised leg than the rested leg. The present findings demonstrate that physical inactivity–induced insulin resistance in muscle is associated with lower content/activity of key proteins in glucose transport/phosphorylation and storage
URI: http://hdl.handle.net/10553/50939
ISSN: 0012-1797
DOI: 10.2337/db11-0884
Fuente: Diabetes[ISSN 0012-1797],v. 61 (5), p. 1090-1099
Colección:Artículos
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