NON-ALCOHOLIC FATTY LIVER DISEASE AND SARCOPENIA
| Autor: | Pivtorak K. V., Marchuk O. V. |
|---|---|
| Jazyk: | English<br />Russian<br />Ukrainian |
| Rok vydání: | 2022 |
| Předmět: | |
| Zdroj: | Вісник проблем біології і медицини, Iss 1, Pp 79--6 (2022) |
| Druh dokumentu: | article |
| ISSN: | 2077-4214 2523-4110 |
| DOI: | 10.29254/2077-4214-2022-3-166-79-86 |
| Popis: | In this paper, an analysis of modern scientific literary sources was carried out regarding common mechanisms of development of sarcopenia and non-alcoholic fatty liver disease. Patients with non-alcoholic liver disease have a high prevalence of sarcopenia, which is characterized by progressive loss of muscle mass and function and affects quality of life and disease prognosis. The article highlights various variants of the pathogenesis of sarcopenia and NAFLD. It is generally known that the liver takes part in the metabolism and accumulation of nutrients, the synthesis and detoxification of many biologically active substances, hormones, cytokines, and ammonia detoxification. Accumulated data indicate that liver dysfunction leads to an imbalance between muscle protein synthesis and its lysis. Other signaling molecules (growth hormone, insulin-like growth factor-1, some myokines) produced in large quantities, as well as oxidative stress, trigger common signaling pathways that promote inflammation and fibrosis. Abdominal and visceral adiposity have been shown to have a strong effect on suppression of growth hormone secretion, and obese patients with the lowest levels of this hormone have the most severe metabolic complications. Therefore, the reduced levels of growth hormone and insulin-like growth factor-1 seen in obese patients may be detrimental to both skeletal muscle and liver, promoting ectopic fat accumulation. Skeletal muscle plays a key role in insulin signaling as the primary tissue responsible for insulin-mediated glucose utilization. Decreased skeletal muscle mass can cause insulin resistance and impaired carbohydrate metabolism, which ultimately leads to NAFLD and its characteristic components and signs. Chronic inflammation and oxidative stress simultaneously cause muscle atrophy and lead to hepatocyte stress reactions, which, in turn, contributes to the progression of liver fibrosis associated with steatohepatitis and nonalcoholic fatty liver disease. A pathogenetic connection between sarcopenia and NAFLD has been established. Numerous studies have proven that aerobic physical exercises, reducing the level of systemic inflammation contribute to reducing the loss of muscle components of body weight and improving clinical and laboratory indicators in NAFLD. |
| Databáze: | Directory of Open Access Journals |
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