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.
Diabetes Alters Contraction-Induced Mitogen Activated Protein Kinase Activation in the Rat Soleus and PlantarisMIIR Faculty Research
Citation InformationKatta, A., Preston, D. L., Karkala, S. K., Asano, S., Meduru, S., Mupparaju, S. P., ... & Blough, E. R. (2008). Diabetes alters contraction-induced mitogen activated protein kinase activation in the rat soleus and plantaris. Experimental Diabetes Research, 2008.