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Exp Neurol. 2013 Oct;248:129-35. doi: 10.1016/j.expneurol.2013.06.003. Epub 2013 Jun 12.

Hibernation: the search for treatments to prevent disuse-induced skeletal muscle atrophy.

Author information

1
Department of Neurobiology, Physiology and Behavior University of California, Davis 95616, USA; Department of Membrane Biology, University of California, Davis 95616, USA. Electronic address: scbodine@ucdavis.edu.

Abstract

Loss of skeletal muscle mass is a serious consequence of multiple diseases and conditions for which there is limited treatment options. Disuse-induced muscle atrophy occurs as the result of both reduced mechanical loading and decreased neural activity. Hibernation represents a unique physiological state where skeletal muscles are protected from unloading, inactivity and nutritional deprivation. A recent study published in Experimental Neurology (Xu et al., 2013) utilized the thirteen-lined ground squirrel, a natural hibernator, to specifically examine whether peroxisome proliferator-activated receptor γ (PPARγ) coactivator 1-α (PGC-1α) and its associated upstream and downstream signaling partners were increased during hibernation. The results showed an increase in PGC-1α expression as well as increases in mitochondrial biogenesis, oxidative capacity, and antioxidant capacity in hibernating animals. It was suggested that upregulation of PCG-1α could be a viable strategy for the treatment of disuse-induced atrophy in humans. This commentary discusses the results of Xu et al. in the context of other studies that have examined muscle sparing in hibernating mammals, and compares these findings to what is known about disuse-induced atrophy in nonhibernating rodents and humans.

PMID:
23769906
DOI:
10.1016/j.expneurol.2013.06.003
[Indexed for MEDLINE]

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