Abstract

The aim of this study was to evaluate the effect of overload-induced hypertrophy on extensor digitorum longus (EDL) and soleus muscles of streptozotocin-induced diabetic rats. The overload-induced hypertrophy and absolute tetanic and twitch forces increases in EDL and soleus muscles were not different between diabetic and control rats. Phospho-Akt and rpS6 contents were increased in EDL muscle after 7 days of overload and returned to the pre-overload values after 30 days. In the soleus muscle, the contents of total and phospho-Akt and total rpS6 were increased in both groups after 7 days. The contents of total Akt in controls and total rpS6 and phospho-Akt in the diabetic rats remained increased after 30 days. mRNA expression after 7 days of overload in the EDL muscle of control and diabetic animals showed an increase in MGF and follistatin and a decrease in myostatin and Axin2. The expression of FAK was increased and of MuRF-1 and atrogin-1 decreased only in the control group, whereas Ankrd2 expression was enhanced only in diabetic rats. In the soleus muscle caused similar changes in both groups: increase in FAK and MGF and decrease in Wnt7a, MuRF-1, atrogin-1, and myostatin. Differences between groups were observed only in the increased expression of follistatin in diabetic animals and decreased Ankrd2 expression in the control group. So, insulin deficiency does not impair the overload-induced hypertrophic response in soleus and EDL muscles. However, different mechanisms seem to be involved in the comparable hypertrophic responses of skeletal muscle in control and diabetic animals.

Highlights

  • Type 1 diabetes (T1DM) is associated with marked changes in skeletal muscle morphology, electrical, and contractile properties and metabolism leading to impaired muscle function (Cotter et al 1989, 1993; Cameron et al 1990; McGuire et al 2001)

  • The contents of total Akt in controls and total ribosomal protein S6 (rpS6) and phospho-Akt in the diabetic rats remained increased after 30 days. mRNA expression after 7 days of overload in the extensor digitorum longus (EDL) muscle of control and diabetic animals showed an increase in Muscle RING-Finger protein-1; IGF-1 Eb (MGF) and follistatin and a decrease in myostatin and Axin2

  • In the overloaded soleus muscle, absolute tetanic force was increased by 107% in the diabetic and by 98% in the control groups

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Summary

Introduction

Type 1 diabetes (T1DM) is associated with marked changes in skeletal muscle morphology, electrical, and contractile properties and metabolism leading to impaired muscle function (Cotter et al 1989, 1993; Cameron et al 1990; McGuire et al 2001). Growth and development of skeletal muscle are impaired in T1DM (Krause et al 2009; D’Souza et al 2013), resulting in reduced myofiber diameter (Andersen et al 1997, 2004) along with lowered capillary density and deficient angiogenesis (Leinonen et al 1982; Krause et al 2009; Rennert et al 2014) These alterations together are diagnosed as diabetic myopathy (Krause et al 2009; D’Souza et al 2013).

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