International journal of molecular sciences · 2026
Circulating Adipokines in Alcohol-Related Liver Disease and MetALD: A Systematic Review and Structured Narrative Synthesis.
СтатьяСистематический обзорНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Mirowski Krystian, Balicka-Ślusarczyk Barbara, Skladany Lubomir, Arab Juan Pablo, Grgurevic Ivica, Kukla Michał
Аннотация
Alcohol-related liver disease (ALD) and metabolic dysfunction and alcohol-related liver disease (MetALD) are increasingly recognised as biologically heterogeneous conditions, but circulating novel adipokines have not been systematically synthesised in this setting. We searched PubMed/MEDLINE, Embase, Web of Science, Scopus and Cochrane CENTRAL from inception to 31 December 2025 for studies measuring chemerin, visfatin/nicotinamide phosphoribosyltransferase (NAMPT), vaspin, omentin-1 or retinol-binding protein 4 (RBP-4) in adults with ALD or MetALD; data were synthesised narratively using Synthesis Without Meta-Analysis (SWiM). Grey literature and non-English databases were not searched, which may have led to incomplete retrieval of small single-centre studies. Five studies were included. Direct ALD evidence came mainly from three cross-sectional alcoholic cirrhosis cohorts, while one population cohort linked baseline RBP-4 to incident MetALD/ALD. RBP-4 showed a phase-dependent pattern, increasing before incident MetALD/ALD but decreasing in established cirrhosis with impaired synthetic function. Chemerin was reduced, omentin-1 was markedly elevated, vaspin was nonspecific and historical visfatin/NAMPT assays were difficult to interpret. Current evidence supports a hypothesis-generating three-axis framework: hepatic source failure, impaired hepatic clearance/portal-systemic shunting and alcohol-driven adipose-liver inflammation. The available evidence chiefly reflects chronic alcohol-related cirrhosis together with limited incident MetALD/ALD risk data, rather than the full ALD/MetALD spectrum. Prospective MetALD-stratified cohorts with isoform-specific assays and objective alcohol biomarkers are required.