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UCHL1 Regulates Lipid and Perilipin 2 Level in Skeletal Muscle
Ryan Antony1, Katherine Aby1, Hongbo Gao1
1Division of Basic Biomedical Sciences, University of South Dakota Sanford School of Medicine, Vermillion, SD, United States.
Frontiers in Physiology
|April 25, 2022
Summary
Ubiquitin C-terminal hydrolase L1 (UCHL1) stabilizes perilipin 2, impacting lipid storage in skeletal muscle. UCHL1 deficiency reduces muscle lipid content and enhances glucose tolerance.
Area of Science:
- Biochemistry
- Cell Biology
- Metabolism
Background:
- Ubiquitin C-terminal hydrolase L1 (UCHL1) is a deubiquitinating enzyme primarily known in neurons.
- UCHL1 is highly expressed in slow oxidative skeletal muscles, but its specific roles there are unclear.
Purpose of the Study:
- To investigate the function of UCHL1 in skeletal muscle metabolism.
- To determine the effect of UCHL1 deficiency on lipid and glucose homeostasis in muscle.
Main Methods:
- Skeletal muscle-selective knockout (smKO) of UCHL1 in mice.
- Analysis of protein levels, lipid content, and glucose tolerance in muscle tissue.
- siRNA knockdown of UCHL1 in C2C12 myotubes.
Main Results:
- UCHL1 protein levels decreased with fasting in skeletal muscle and glucose starvation in C2C12 myotubes.
- UCHL1 smKO significantly reduced skeletal muscle lipid content and improved glucose tolerance.
- Perilipin 2 levels were significantly downregulated in UCHL1-deficient muscle and myotubes, while major lipases and transporters remained unchanged.
Conclusions:
- UCHL1 plays a role in regulating lipid storage in skeletal muscle.
- UCHL1 may stabilize perilipin 2, contributing to lipid accumulation in muscle.
- Targeting UCHL1 could be a strategy for managing metabolic disorders related to lipid storage.
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