Hypertrophy Stimulation at the Onset of Type I Diabetes Maintains the Soleus but Not the EDL Muscle Mass in Wistar Rats.

Fortes MAS, Scervino MVM, Marzuca-Nassr GN, Vitzel KF, da Justa Pinheiro CH, Curi R

Frontiers in physiology26 Oct 2017Cited by 10 (Europe PMC)

PMID29123487PMCIDPMC5662641DOI10.3389/fphys.2017.00830PepBankPUB-29123487

Summary

Diabetes mellitus induces a reduction in skeletal muscle mass and strength. Strength training is prescribed as part of treatment since it improves glycemic control and promotes increase of skeletal muscle mass. The mechanisms involved in overload-induced muscle hypertrophy elicited at the establishment of the type I diabetic state was investigated in Wistar rats. The purpose was to examine whether the overload-induced hypertrophy can counteract the hypotrophy associated to the diabetic state. The experiments were performed in oxidative (soleus) or glycolytic (EDL) muscles. PI3K/Akt/mTOR protein synthesis pathway was evaluated 7 days after overload-induced hypertrophy of soleus and of EDL muscles. The mRNA expression of genes associated with different signaling pathways that control muscle hypertrophy was also evaluated: mechanotransduction (FAK), Wnt/β-catenin, myostatin, and follistatin. The soleus and EDL muscles when submitted to overload had similar hypertrophic responses in control and diabetic animals. The increase of absolute and specific twitch and tetanic forces had the same magnitude as muscle hypertrophic response. Hypertrophy of the EDL muscle from diabetic animals mostly involved mechanical loading-stimulated PI3K/Akt/mTOR pathway besides the reduced activation of AMP-activated protein kinase (AMPK) and decrease of myostatin expression. Hypertrophy was more pronounced in the soleus muscle of diabetic animals due to a more potent activation of rpS6 and increased mRNA expression of insulin-like growth factor-1 (IGF-1), mechano-growth factor (MGF) and follistatin, and decrease of myostatin, MuRF-1 and atrogin-1 contents. The signaling changes enabled the soleus muscle mass and force of the diabetic rats to reach the values of the control group.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

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01AnimalEndogenous levelAnimal study (in vivo)Mechanism
In diabetic Wistar rats, overload-induced hypertrophy of the soleus muscle was accompanied by increased mRNA expression of the body's own MGF, together with IGF-1 and follistatin.
In plain wordsIn diabetic rats, muscle overload raised the body's own MGF gene activity in the soleus muscle.
Peptide
MGF / PEG-MGF
Outcome
IncreaseMGF mRNA expression in overloaded soleus of diabetic rats
Study
ratn: not reported in source
Wistar rats with type I diabetes, overload-induced hypertrophy
Outcome group
Muscle injury and repair · Musculoskeletal
Source sentences
Summary
increased mRNA expression of insulin-like growth factor-1 (IGF-1), mechano-growth factor (MGF) and follistatin
1 context sentence(design, population, supporting numbers)
Summary · context
The mechanisms involved in overload-induced muscle hypertrophy elicited at the establishment of the type I diabetic state was investigated in Wistar rats.
This result measures the body's own MGF / PEG-MGF. Nobody was given the peptide. It is not evidence about taking it.
Show in the study text Report a problemFND-2912348701

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Version history

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Version 2Current
13 Oct 2026, 21:44 UTC
Study results updated
Version 1
13 Oct 2026, 16:31 UTC
First added · source update from Europe PMC

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