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Exp Diabetes Res ; 2008: 738101, 2008.
Article in English | MEDLINE | ID: mdl-18551177

ABSTRACT

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.


Subject(s)
Diabetes Mellitus, Experimental/pathology , Diabetes Mellitus/pathology , Gene Expression Regulation, Enzymologic , MAP Kinase Signaling System , Muscle Contraction , Muscle, Skeletal/metabolism , Muscle, Skeletal/pathology , Animals , Diabetes Mellitus/enzymology , Diabetes Mellitus, Experimental/enzymology , Male , Phosphorylation , Physical Conditioning, Animal , Rats , Rats, Zucker , Signal Transduction
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