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Updated: Jan 18, 2026

Tibial Nerve Transection - A Standardized Model for Denervation-induced Skeletal Muscle Atrophy in Mice

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Published on: November 3, 2013

O-GlcNAcase Inhibitor Improves Denervation-Induced Muscle Atrophy in Mice.

Tomoyasu Suenaga^1,2, Shouji Matsushima^1,2, Tomoka Masunaga^1,2

¹Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.

Journal of Cachexia, Sarcopenia and Muscle

|September 12, 2025

Summary

This summary is machine-generated.

Inhibition of O-GlcNAcase, an enzyme involved in O-linked N-acetylglucosamine modification, can prevent muscle atrophy. This approach increases Akt phosphorylation, a key factor in maintaining muscle mass.

Keywords:

O‐GlcNAcase O‐GlcNAcylation denervation‐induced muscle atrophy phosphorylation skeletal muscle thiamet G

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Area of Science:

Biochemistry
Molecular Biology
Physiology

Background:

Skeletal muscle atrophy, characterized by muscle wasting, is linked to an imbalance in protein synthesis and degradation.
Impaired Akt phosphorylation is a critical factor in muscle atrophy.
O-linked N-acetylglucosamine (O-GlcNAcylation) is a post-translational modification that regulates protein function and interacts with Akt phosphorylation.

Purpose of the Study:

To investigate the role of O-GlcNAcylation in skeletal muscle atrophy.
To identify O-GlcNAcase as a potential therapeutic target for preventing muscle atrophy.

Main Methods:

Denervation-induced skeletal muscle atrophy model in mice.
Treatment with O-GlcNAcase inhibitor (thiamet G) or vehicle.
Analysis of muscle weight, Akt phosphorylation, O-GlcNAcylation, and expression of atrophy markers (atrogin-1, MuRF1).
Investigated the effect of O-GlcNAcase gene silencing and Akt mutant overexpression in C2C12 myotubes.

Main Results:

Denervation significantly decreased muscle weight, Akt phosphorylation, and Akt O-GlcNAcylation, while increasing atrogin-1 and MuRF1 expression.
Thiamet G treatment attenuated muscle weight loss, increased Akt phosphorylation, and reduced atrogin-1 and MuRF1 expression.
O-GlcNAcase inhibition via gene silencing also improved muscle atrophy.
Overexpression of a phosphorylation-resistant Akt mutant showed reduced O-GlcNAcase inhibition-induced Akt phosphorylation.

Conclusions:

Inhibition of O-GlcNAcase effectively ameliorates denervation-induced skeletal muscle atrophy in mice.
This therapeutic effect is mediated by increased Akt O-GlcNAcylation and subsequent enhancement of Akt phosphorylation.
O-GlcNAcase represents a promising therapeutic target for the prevention of skeletal muscle atrophy.