Table of Contents Author Guidelines Submit a Manuscript
Experimental Diabetes Research
Volume 2008, Article ID 738101, 10 pages
Research Article

Diabetes Alters Contraction-Induced Mitogen Activated Protein Kinase Activation in the Rat Soleus and Plantaris

1Department of Biological Sciences, Marshall University, Huntington, WV 25755, USA
2Department of Exercise Science and Sports Recreation, Marshall University, Huntington, WV 25755, USA
3Departments of Pharmacology, Physiology, and Toxicology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755, USA
4Cell Differentiation and Development Center, Marshall University, Huntington, WV 25755, USA

Received 15 February 2007; Revised 1 July 2007; Accepted 24 February 2008

Academic Editor: Ryichi Kikkawa

Copyright © 2008 A. Katta et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The prescription of anaerobic exercise has recently been advocated for the management of diabetes; however exercise-induced signaling in diabetic muscle remains largely unexplored. Evidence from exercise studies in nondiabetics suggests that the extracellular-signal-regulated kinases (Erk1/2), p38, and c-JUN NH2-terminal kinase (Jnk) mitogen-activated protein kinases (MAPKs) are important regulators of muscle adaptation. Here, we compare the basal and the in situ contraction-induced phosphorylation of Erk1/2- p38- and Jnk-MAPK and their downstream targets (p90rsk and MAPKAP-K2) in the plantaris and soleus muscles of normal and obese (fa/fa) Zucker rats. Compared to lean animals, the time course and magnitude of Erk1/2, p90rsk and p38 phosphorylation to a single bout of contractile stimuli were greater in the plantaris of obese animals. Jnk phosphorylation in response to contractile stimuli was muscle-type dependent with greater increases in the plantaris than the soleus. These results suggest that diabetes alters intramuscular signaling processes in response to a contractile stimulus.