Zahrawi Frhaan, Suyavaran Arumugam, Banini Bubu A, Mehal Wajahat Z
The Section of Digestive Diseases, Yale School of Medicine, New Haven, CT, USA.
West Haven Veterans Medical Center, New Haven, CT, USA.
NPJ Metab Health Dis. 2025 Sep 18;3(1):36. doi: 10.1038/s44324-025-00077-y.
Glucagon-like peptide 1 receptor (GLP-1R) agonists are used along with ethanol consumption, but their interactions are not understood. Our aim was to determine the effects of GLP-1R agonism on the liver in mouse models of high ethanol consumption. We identified that GLP-1R agonism reduced ethanol consumption, mitigated ethanol-induced upregulation of several liver metabolizing enzymes, including Cyp2e1 and also reduced Cyp2e1 independent of ethanol intake. As expected from a reduction in Cyp2e1, GLP-1R agonism resulted in increased blood ethanol levels. This occurred after a single dose of ethanol when given by gavage, and by the intraperitoneal route. This suggests that GLP-1R agonism can reduce ethanol-mediated hepatotoxicity despite continued ethanol consumption and elevate blood alcohol levels.
胰高血糖素样肽1受体（GLP-1R）激动剂与乙醇消耗同时使用，但其相互作用尚不清楚。我们的目的是确定GLP-1R激动作用在高乙醇消耗小鼠模型中对肝脏的影响。我们发现，GLP-1R激动作用可减少乙醇消耗，减轻乙醇诱导的几种肝脏代谢酶（包括Cyp2e1）的上调，并且与乙醇摄入量无关地降低Cyp2e1。正如Cyp2e1减少所预期的那样，GLP-1R激动作用导致血液乙醇水平升高。这在通过灌胃和腹腔途径给予单剂量乙醇后发生。这表明，尽管持续乙醇消耗，GLP-1R激动作用仍可降低乙醇介导的肝毒性并提高血液酒精水平。
