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J Appl Physiol 101: 1368-1376, 2006. First published June 29, 2006; doi:10.1152/japplphysiol.00416.2006
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Increased submaximal insulin-stimulated glucose uptake in mouse skeletal muscle after treadmill exercise

Taku Hamada, Edward B. Arias, and Gregory D. Cartee

Muscle Biology Laboratory, Division of Kinesiology, University of Michigan, Ann Arbor, Michigan

Submitted 7 April 2006 ; accepted in final form 21 June 2006

The primary purpose of this study was to determine the effect of prior exercise on insulin-stimulated glucose uptake with physiological insulin in isolated muscles of mice. Male C57BL/6 mice completed a 60-min treadmill exercise protocol or were sedentary. Paired epitrochlearis, soleus, and extensor digitorum longus (EDL) muscles were incubated with [3H]-2-deoxyglucose without or with insulin (60 µU/ml) to measure glucose uptake. Insulin-stimulated glucose uptake for paired muscles was calculated by subtracting glucose uptake without insulin from glucose uptake with insulin. Muscles from other mice were assessed for glycogen and AMPK Thr172 phosphorylation. Exercised vs. sedentary mice had decreased glycogen in epitrochlearis (48%, P < 0.001), soleus (51%, P < 0.001), and EDL (41%, P < 0.01) and increased AMPK Thr172 phosphorylation (P < 0.05) in epitrochlearis (1.7-fold), soleus (2.0-fold), and EDL (1.4-fold). Insulin-independent glucose uptake was increased 30 min postexercise vs. sedentary in the epitrochlearis (1.2-fold, P < 0.001), soleus (1.4-fold, P < 0.05), and EDL (1.3-fold, P < 0.01). Insulin-stimulated glucose uptake was increased (P < 0.05) ~85 min after exercise in the epitrochlearis (sedentary: 0.266 ± 0.045 µmol·g–1·15 min–1; exercised: 0.414 ± 0.051) and soleus (sedentary: 0.102 ± 0.049; exercised: 0.347 ± 0.098) but not in the EDL. Akt Ser473 and Akt Thr308 phosphorylation for insulin-stimulated muscles did not differ in exercised vs. sedentary. These results demonstrate enhanced submaximal insulin-stimulated glucose uptake in the epitrochlearis and soleus of mice 85 min postexercise and suggest that it will be feasible to probe the mechanism of enhanced postexercise insulin sensitivity by using genetically modified mice.

glucose transport; exertion; insulin sensitivity; Akt; AMP-activated protein kinase



Address for reprint requests and other correspondence: G. D. Cartee, Univ. of Michigan, Division of Kinesiology, Rm. 3040E, 401 Washtenaw Ave., Ann Arbor, MI 48109-2214 (e-mail: gcartee{at}umich.edu)




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J.-S. Ju, M. A. Gitcho, C. A. Casmaer, P. B. Patil, D.-G. Han, S. A. Spencer, and J. S. Fisher
Potentiation of insulin-stimulated glucose transport by the AMP-activated protein kinase
Am J Physiol Cell Physiol, January 1, 2007; 292(1): C564 - C572.
[Abstract] [Full Text] [PDF]




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