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

Yaspelkis, B, Lessard, S, Reeder, D, Limon, J, Saito, M, Rivas, D, Kvasha, I and Hawley, J 2007, 'Exercise reverses high-fat diet-induced impairments on compartmentalization and activation of components of the insulin-signaling cascade in skeletal muscle', American Journal of Physiology - Endocrinology and Metabolism, vol. 293, no. 4, pp. E941-E949.


Document type: Journal Article
Collection: Journal Articles

Title Exercise reverses high-fat diet-induced impairments on compartmentalization and activation of components of the insulin-signaling cascade in skeletal muscle
Author(s) Yaspelkis, B
Lessard, S
Reeder, D
Limon, J
Saito, M
Rivas, D
Kvasha, I
Hawley, J
Year 2007
Journal name American Journal of Physiology - Endocrinology and Metabolism
Volume number 293
Issue number 4
Start page E941
End page E949
Total pages 9
Publisher American Physiological Society
Abstract 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.
Subject Medical Physiology not elsewhere classified
Keyword(s) Protein-Kinase-C
Obese Zucker Rats
Stimulated Phosphatidylinositol 3-Kinase
Glucose-Transport
Rosiglitazone Treatment
Plasma-Membrane
Glut4 Vesicles
Adipose-Cells
Resistance
Translocation
DOI - identifier 10.1152/ajpendo.00230.2007
Copyright notice © 2007 American Physiological Society
ISSN 0193-1849
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