ABSTRACT
Chronic alcoholic myopathy occurs in 40-60% of patients who abuse alcohol, and is accompanied by decreased performance, proximal paresis and atrophy of skeletal muscles. However, it is unknown what is important in the development of the disease: duration of alcohol abuse, or the dose of ethanol consumed. Unknown dynamics of the pathological process in skeletal muscle. We examined male patients identified with alcoholic myopathy and without it, evaluated the duration of alcohol abuse, intake of ethanol, morphological characteristics m.quadriceps vastus lateralis and the content of IGF-1 in plasma. It has been shown that chronic alcoholic myopathy develops after 10 years of alcohol abuse; proximal paresis is observed only in patients with atrophy of muscle fibers, thus there is a transformation of myosin phenotype from slow to fast. The decrease IGF-1 in plasma detected at the early stages of the Church, including in patients without clinical manifestations of proximal paresis and morphological signs of atrophy of muscle fibers.
Subject(s)
Alcoholic Intoxication/physiopathology , Muscular Diseases/physiopathology , Adult , Alcoholic Intoxication/blood , Alcoholism/blood , Alcoholism/physiopathology , Ethanol/toxicity , Humans , Insulin-Like Growth Factor I/metabolism , Male , Middle Aged , Muscle, Skeletal/drug effects , Muscle, Skeletal/physiopathology , Muscular Diseases/blood , Muscular Diseases/chemically inducedABSTRACT
Chronic alcoholic myopathy is one of most numerous and profound manifestations of chronic alcohol intoxication. This disease is characterized by the pronounced atrophy of the locomotor muscles, which involves predominantly those fibers expressing myosin isoforms of the I "fast" type. In early experiments with alcohol-fed rats and studies of patients it was shown the impairment of the anabolic intracellular signaling pathways and decrease in protein synthesis rate. We were the first to analyze the signaling pathways involved in the pathogenesis of alcoholic myopathy with different fiber atrophy levels. At the early stages of the pathogenesis we observed also the sufficient increase of mRNA of E3 ubiquitin ligases. However the ubiquitinylation level was not altered in patients as compared to the control subjects. This phenomenon could be associated with the increased expression of the heat-shock proteins, known for their protective action.
