3 years ago

Effect of chronic alcohol abuse on anabolic and catabolic signaling pathways in human skeletal muscle

Tatiana L. Nemirovskaya, Svetlana P. Belova, Olga E. Zinovyeva, Tatiana Y. Kostrominova, Nudlya D. Samkhaeva, Boris S. Shenkman, Olga V. Turtikova, Timur M. Mirzoev, Erzhena G. Altaeva, Natalia A. Vilchinskaya
Background Animal studies showed that alcoholic myopathy is characterized by the reduction of myofiber cross sectional area (CSA) and by impaired anabolic signaling. The goal of the current study was to compare changes in CSA and fiber type composition with modifications in anabolic and catabolic signaling pathways at the early stages of alcohol misuse in humans. Methods Skeletal muscle samples from seven male patients with chronic alcohol abuse (AL; 47.7±2.0 years old; alcohol misuse duration 7.7±0.6 years) were compared with muscle from control group of seven healthy men (C; 39.7±5.0 years old). Biopsies from vastus lateralis muscles were taken and analyzed for the changes in fiber type composition, fiber CSA, and for the alterations in anabolic and catabolic signaling pathways. Results AL patients did not have detectable clinical myopathy symptoms or muscle fiber atrophy, but the relative proportion of fast fibers was increased. There was a significant decrease of IGF-I in plasma and IRS-1 protein content in muscle of AL group. Levels of total and phosphorylated p70S6K1, GSK3β, and p90RSK1 were not different between AL and C groups. Muscle of AL patients had increased mRNA expression of HSP70 and HSP90. A marker of anabolic pathway p-4E-BP1 was decreased while catabolic markers (MuRF-1, MAFbx, ubiquitinated proteins) were increased in AL patients when compared with C group. Conclusions At the early stages of alcohol misuse in humans, changes in the regulation of anabolic and catabolic signaling pathways precede the development of skeletal muscle atrophy and manifestation of clinical symptoms of alcoholic myopathy. This article is protected by copyright. All rights reserved.

Publisher URL: http://onlinelibrary.wiley.com/resolve/doi

DOI: 10.1111/acer.13531

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