Abstract
Skeletal muscle dysfunction is highly prevalent and is one of the earliest pathological tissue changes among people with at-risk alcohol use. Clinical studies to elucidate pathophysiological mechanisms of alcohol-mediated muscle disease are hampered due to ethical considerations, and confounded by nutritional, lifestyle, and comorbid conditions. Rodent models have been developed to study the impact of at-risk alcohol consumption and alcohol-mediated end organ injury, including skeletal muscle dysfunction. This review discusses results from well-established rodent models of alcohol administration and highlights key pathophysiological mechanisms underlying alcoholic myopathy identified in rodent models. Salient pathways include impaired regenerative capacity, altered anabolic/catabolic balance, impaired mitochondrial bioenergetic function, and skeletal muscle morphological and contractile changes.
Highlights
Skeletal muscle dysfunction is highly prevalent and is one of the earliest pathological tissue changes among people with at-risk alcohol use
There is strong evidence that alcohol attenuates basal mammalian target of rapamycin (mTOR) signaling after chronic administration, acutely attenuates mTOR signaling in response to anabolic stimulation, and may decrease systemic levels of the anabolic hormone, insulin-like growth factor (IGF)-1
Studies in rodent models suggest that alcohol-mediated decreased protein synthesis and increased protein degradation can potentially contribute to alcoholic myopathy
Summary
Journal of Veterinary and Animal Sciences ISSN (Print): 0971-0701, (Online): 2582-0605 https://doi.org/10.51966/jvas.2021.52.2.107-116 Pathophysiological mechanisms of alcoholic myopathy - Lessons from rodent models Danielle E. Levitt1, Patricia E. Molina2 and Liz Simon3 Department of Physiology, Louisiana State University Health Sciences Center, 1901 Perdido Citation: Levitt, D. E., Molina, P. E. and Simon, L. 2021. Pathophysiological mechanisms of alcoholic myopathy: Lessons from rodent models. J. Vet. Ani. Sci. 52 (2): 107-116. DOI: https://doi.org/10.51966/jvas.2021.52.2.107-116
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