Akt expression is diminished by physical inactivity in early stages of development in soleus muscle of rats La inactividad física en etapas tempranas del desarrollo disminuye la expresión de akt en el músculo sóleo de ratas

Marquez J.L.; Hirabara S.M.; Fiamoncini J.; Hatanaka; E; Alba-Loureiro T.C.; de Lima-Salgado T.M.; Curi R.; Salazar, L.A.


Metabolic Syndrome is a group of conditions related to obesity and physical inactivity. Little is known about the role of physical inactivity, in early stages of development, in the susceptibility to insulin resistant phenotype induced by high fat diet. Akt plays a key role in protein synthesis and glucose transport in skeletal muscle and has been regulated by muscle activity. The objective of present study was to determine the effect of early physical inactivity on muscle growth and susceptibility to acquire a diabetic phenotype and to assess its relationship with Akt expression. Forty Wistar male rats were distributed in two groups (standard group, Std) and movement restriction (RM). Between days 23 and 70 after birth, RM group was kept in small cages that did not allow them to perform relevant motor activity. From day 71 to 102 after birth, 10 rats of each group were fed with hyperlipidic diet (groups Std-DAG and RMDAG). No differences were observed in total body weight although DAG increased epididymal fat pad weight. RM decreased significantly the soleus weight. Insulin-mediated glucose uptake was lower in RM-DAG group. Akt protein levels were lower in RM groups. Real time RT-PCR analysis showed that movement restriction decreased mRNA levels of AKT1 in soleus muscle, regardless of supplied diet. These findings suggest that early physical inactivity limits muscle's growth and contributes to instauration of insulin resistant phenotype, which can be partly explained by dysregulation of Akt expression.

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Título de la Revista: International Journal of Morphology
Volumen: 29
Número: 1
Editorial: Dr. Mariano Del Sol. Universidad de la Frontera, Chile.
Fecha de publicación: 2011
Página de inicio: 256
Página final: 267
URL: http://www.scopus.com/inward/record.url?eid=2-s2.0-79957452251&partnerID=q2rCbXpz