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Related Experiment Video

Updated: May 12, 2026

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer

Published on: November 15, 2024

Aging accentuates alcohol-induced decrease in protein synthesis in gastrocnemius.

Donna H Korzick¹, Daniel R Sharda, Anne M Pruznak

¹Department of Kinesiology, The Pennsylvania State University, University Park, PA, USA.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology

|March 29, 2013

Summary

Aging exacerbates alcohol

Keywords:

AMPK atrophy mTOR protein degradation sarcopenia

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Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer

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Disruption of Frontal Lobe Neural Synchrony During Cognitive Control by Alcohol Intoxication

Disruption of Frontal Lobe Neural Synchrony During Cognitive Control by Alcohol Intoxication

Published on: February 6, 2019

Area of Science:

Gerontology
Molecular Biology
Nutritional Science

Background:

Aging is associated with muscle loss and altered protein metabolism.
Chronic alcohol consumption can induce muscle catabolism.
The combined effects of aging and alcohol on muscle protein synthesis and degradation are not fully understood.

Purpose of the Study:

To investigate if aged rats exhibit an exaggerated protein catabolic response in skeletal muscle following chronic alcohol feeding compared to adult rats.
To elucidate the molecular mechanisms underlying alcohol-induced muscle catabolism in aging, focusing on protein synthesis and degradation pathways.

Main Methods:

Adult (3-month-old) and aged (18-month-old) female F344 rats were fed alcohol or control diets for 20 weeks.
Gastrocnemius muscle was analyzed for protein synthesis, mTOR and proteasome activity, and key signaling pathway components (e.g., IGF-I, TNF-α, IL-6, AMPK, 4E-BP1, Raptor).
Lean body mass and circulating IGF-I were also measured.

Main Results:

Aged rats showed an exaggerated alcohol-induced reduction in lean body mass and gastrocnemius protein synthesis compared to adult rats.
Alcohol-fed aged rats exhibited altered mTOR signaling (e.g., 4E-BP1 dephosphorylation, altered Raptor binding) and upregulation of the LKB1-AMPK-REDD1 pathway.
While alcohol exacerbated muscle protein synthesis decline in aged rats, it did not further increase inflammatory mediators or age-related increases in atrogin-1/MuRF1 mRNA or proteasome activity.

Conclusions:

Skeletal muscle in aged rats is more sensitive to the catabolic effects of alcohol on protein synthesis than in adult rats.
The exaggerated catabolic response in aged rats appears to be linked to muscle-specific insulin-like growth factor-I (IGF-I) reduction and potentially mediated by the AMPK pathway.
Alcohol's impact on protein degradation pathways (atrogin-1, MuRF1, proteasome) was not exaggerated by aging in this study.