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This Article Full Text Full Text (PDF) All Versions of this Article: 293/4/E941    most recent 00230.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Yaspelkis, B. B. Articles by Hawley, J. A. Search for Related Content PubMed PubMed Citation Articles by Yaspelkis, B. B., III Articles by Hawley, J. A.

Exercise reverses high-fat diet-induced impairments on compartmentalization and activation of components of the insulin-signaling cascade in skeletal muscle

¹Exercise Biochemistry Laboratory, Department of Kinesiology, California State University Northridge, Northridge, California; and ²Exercise Metabolism Group, School of Medical Sciences, Royal Melbourne Institute of Technology University, Bundoora, Victoria, Australia

Submitted 12 April 2007 ; accepted in final form 2 July 2007

The aims of this investigation were 1) to determine whether endurance exercise training could reverse impairments in insulin-stimulated compartmentalization and/or activation of aPKC/ and Akt2 in skeletal muscle from high-fat-fed rodents and 2) to assess whether the PPAR agonist rosiglitazone could reverse impairments in skeletal muscle insulin signaling typically observed after high-fat feeding. Sprague-Dawley rats were placed on chow (NORCON, n = 16) or high-fat (n = 64) diets for 4 wk. During a subsequent 4-wk experimental period, high-fat-fed rats were allocated (n = 16/group) to either sedentary control (HFC), exercise training (HFX), rosiglitazone treatment (HFRSG), or a combination of both exercise training and rosiglitazone (HFRX). Following the 4-wk experimental period, animals underwent hindlimb perfusions. Insulin-stimulated plasma membrane-associated aPKC and - protein concentration, aPKC/ activity, GLUT4 protein concentration, cytosolic Akt2, and aPKC/ activities were reduced (P < 0.05) in HFC compared with NORCON. Cytosolic Akt2, aPKC, and aPKC protein concentrations were not affected in HFC compared with NORCON. Exercise training reversed the deleterious effects of the high-fat diet such that insulin-stimulated compartmentalization and activation of components of the insulin-signaling cascade in HFX were normalized to NORCON. High-fat diet-induced impairments to skeletal muscle glucose metabolism were not reversed by rosiglitazone administration, nor did rosiglitazone augment the effect of exercise. Our findings indicate that chronic exercise training, but not rosiglitazone, reverses high-fat diet induced impairments in compartmentalization and activation of components of the insulin-signaling cascade in skeletal muscle.

rosiglitazone; Akt2 and atypical protein kinase C/ activities; Akt2, atypical protein kinase C, atypical protein kinase C, and glucose transporter 4 protein concentrations