Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease that can progress to fibrosis, cirrhosis, and liver cancer. The liver interacts with other organs by releasing hepatokines — hormone‑like proteins that are mainly secreted by hepatocytes. The first identified hepatokine that regulates human metabolic homeostasis through multiorgan interactions is fetuin‑A — a multifunctional α2‑glycoprotein that belongs to the family of cystatin protease inhibitors. Experimental and clinical studies have demonstrated a significant increase in circulating fetuin‑A in metabolically associated diseases, including obesity, type 2 diabetes, and nonalcoholic fatty liver disease. The review demonstrated that fetuin‑A correlates with many parameters associated with dysregulation of metabolic homeostasis, such as insulin sensitivity, glucose tolerance, circulating lipid levels, as well as markers of systemic inflammation (C‑reactive protein, tumor necrosis factor α (TNF‑α) and interleukin (IL)‑6). The results of the effects of fetuin‑A on the processes of fibrosis in liver tissue are given. In particular, fetuin‑A has been shown to inhibit the signaling of transforming growth factor‑β1, which promotes fibrotic changes in many tissues, including the liver, blood vessels, which indicates the ability of fetuin‑A to prevent fibrotic changes in these organs. The influence of non‑drug and drug treatment methods of NAFLD on the dynamics of fetuin‑A levels was analyzed. It has been shown that physical activity does not significantly affect the dynamics of fetuin‑A, while metformin, thiazolidinediones and probiotics reduce the level of this hepatokine and normalize metabolic disorders. Further study of the role of fetuin‑A in the pathophysiological process of NAFLD may open new perspectives in early diagnosis, identification of new biomarkers, and provision of new targets for pharmacological interventions.
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