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Title: GLUT4 and glycogen synthase are key players in bed rest-induced insulin resistance
Authors: 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.
UNESCO Clasification: 241106 Fisiología del ejercicio
Keywords: Human Skeletal-Muscle
Exercise-Induced Increase
Stimulated Phosphorylation
Gene-Expression, et al
Issue Date: 2012
Publisher: 0012-1797
Journal: Diabetes (New York, N.Y.) 
Abstract: 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
ISSN: 0012-1797
DOI: 10.2337/db11-0884
Source: Diabetes[ISSN 0012-1797],v. 61 (5), p. 1090-1099
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