Rac1 governs exercise-stimulated glucose uptake in skeletal muscle through regulation of GLUT4 translocation in mice
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Rac1 governs exercise-stimulated glucose uptake in skeletal muscle through regulation of GLUT4 translocation in mice. / Sylow, Lykke; Laurent, Ida; Kleinert, Maximilian; Møller, Lisbeth Liliendal Valbjørn; Ploug, Thorkil; Schjerling, Peter; Bilan, Philip J.; Klip, Amira; Jensen, Thomas Elbenhardt; Richter, Erik A.
I: Journal of Physiology, Bind 594, Nr. 17, 2016, s. 4997-5008.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Rac1 governs exercise-stimulated glucose uptake in skeletal muscle through regulation of GLUT4 translocation in mice
AU - Sylow, Lykke
AU - Laurent, Ida
AU - Kleinert, Maximilian
AU - Møller, Lisbeth Liliendal Valbjørn
AU - Ploug, Thorkil
AU - Schjerling, Peter
AU - Bilan, Philip J.
AU - Klip, Amira
AU - Jensen, Thomas Elbenhardt
AU - Richter, Erik A.
N1 - CURIS 2016 NEXS 186
PY - 2016
Y1 - 2016
N2 - Exercise increase skeletal muscle energy turnover and one of the important substrates for the working muscle is glucose taken up from the blood. Despite extensive efforts, the signaling mechanisms vital for glucose uptake during exercise are not yet fully understood but the GTPase Rac1 is a candidate molecule. This study investigated the role of Rac1 in muscle glucose uptake and substrate utilization during treadmill exercise in mice in vivo. Exercise-induced uptake of radiolabelled 2-deoxyglucose (2-DG) at 65% max running capacity was blocked in soleus and decreased by 80 and 60% in gastrocnemius and tibialis anterior muscles, respectively, in muscle-specific inducible Rac1 knockout (mKO) mice compared to wildtype littermates. By developing an assay to quantify endogenous GLUT4 translocation, we observed that GLUT4 content at the sarcolemma in response to exercise was reduced in Rac1 mKO muscle. Our findings implicate Rac1 as a regulatory element critical for controlling glucose uptake during exercise via regulation of GLUT4 translocation. This article is protected by copyright. All rights reserved.
AB - Exercise increase skeletal muscle energy turnover and one of the important substrates for the working muscle is glucose taken up from the blood. Despite extensive efforts, the signaling mechanisms vital for glucose uptake during exercise are not yet fully understood but the GTPase Rac1 is a candidate molecule. This study investigated the role of Rac1 in muscle glucose uptake and substrate utilization during treadmill exercise in mice in vivo. Exercise-induced uptake of radiolabelled 2-deoxyglucose (2-DG) at 65% max running capacity was blocked in soleus and decreased by 80 and 60% in gastrocnemius and tibialis anterior muscles, respectively, in muscle-specific inducible Rac1 knockout (mKO) mice compared to wildtype littermates. By developing an assay to quantify endogenous GLUT4 translocation, we observed that GLUT4 content at the sarcolemma in response to exercise was reduced in Rac1 mKO muscle. Our findings implicate Rac1 as a regulatory element critical for controlling glucose uptake during exercise via regulation of GLUT4 translocation. This article is protected by copyright. All rights reserved.
U2 - 10.1113/JP272039
DO - 10.1113/JP272039
M3 - Journal article
C2 - 27061726
VL - 594
SP - 4997
EP - 5008
JO - The Journal of Physiology
JF - The Journal of Physiology
SN - 0022-3751
IS - 17
ER -
ID: 161001827