Metabolism open · 2026
Therapeutic modulation of the gut-brain axis in alcohol use disorder: A systematic review.
СтатьяНазвание 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.
Bhandari Prabha, Sideeg Abdelhaleem, Elfeki Mohamed, Xie Chencheng, Singal Ashwani K
Аннотация
BACKGROUND: Alcohol Use Disorder (AUD) involves gut-brain axis dysfunction. Modulating microbiota offers a promising therapeutic strategy.
METHODS: Clinical trials on fecal microbiota transplant (FMT), prebiotics (inulin), probiotics, and neurohormonal agents like glucagon-like peptide-1 (GLP-1) and ghrelin receptor antagonists) were identified through PubMed, Google Scholar, Scopus, and ClinicalTrials.gov (until 07/31/2026). Of the eleven included studies, five identified gut dysbiosis as a common feature in individuals with AUD.
RESULTS: Gut dysbiosis-directed interventions were associated with benefits on behavioral (alcohol craving, consumption, relapse), psychological (anxiety, sociability), and physiological (MELD score, AST/ALT ratio, systemic inflammation) outcomes. However, the magnitude and consistency of these effects varied among studies. Three studies specifically involved AUD patients with alcohol-associated liver disease (ALD), while the others focused on AUD. In another study, Ghrelin, which was investigated as a neurohormonal target, emerged as a potential anti-inflammatory agent. However, ghrelin receptor antagonism in the presence of alcohol did not alter systemic inflammation. Of five trials using GLP-1 receptor agonists, three showed a reduction in alcohol use, but the other two, although directionally consistent, did not reach statistically significant effects. The current evidence supports the gut-brain axis as a dual therapeutic target, offering potential benefits for both AUD and ALD. Microbial therapies (FMT, probiotics, prebiotics) show some benefits in AUD, albeit studies are small. Hormonal targets such as ghrelin and GLP-1 receptors are mechanistically relevant. Data on ghrelin are limited. Data on GLP-1 receptor agonists are directionally consistent but not statistically robust. Large-scale, controlled trials are needed to validate and optimize the integration of this approach into AUD treatment strategies.
METHODS: Clinical trials on fecal microbiota transplant (FMT), prebiotics (inulin), probiotics, and neurohormonal agents like glucagon-like peptide-1 (GLP-1) and ghrelin receptor antagonists) were identified through PubMed, Google Scholar, Scopus, and ClinicalTrials.gov (until 07/31/2026). Of the eleven included studies, five identified gut dysbiosis as a common feature in individuals with AUD.
RESULTS: Gut dysbiosis-directed interventions were associated with benefits on behavioral (alcohol craving, consumption, relapse), psychological (anxiety, sociability), and physiological (MELD score, AST/ALT ratio, systemic inflammation) outcomes. However, the magnitude and consistency of these effects varied among studies. Three studies specifically involved AUD patients with alcohol-associated liver disease (ALD), while the others focused on AUD. In another study, Ghrelin, which was investigated as a neurohormonal target, emerged as a potential anti-inflammatory agent. However, ghrelin receptor antagonism in the presence of alcohol did not alter systemic inflammation. Of five trials using GLP-1 receptor agonists, three showed a reduction in alcohol use, but the other two, although directionally consistent, did not reach statistically significant effects. The current evidence supports the gut-brain axis as a dual therapeutic target, offering potential benefits for both AUD and ALD. Microbial therapies (FMT, probiotics, prebiotics) show some benefits in AUD, albeit studies are small. Hormonal targets such as ghrelin and GLP-1 receptors are mechanistically relevant. Data on ghrelin are limited. Data on GLP-1 receptor agonists are directionally consistent but not statistically robust. Large-scale, controlled trials are needed to validate and optimize the integration of this approach into AUD treatment strategies.