The long pursuit of effective therapies for AUD has produced surprisingly few successes—only three medications are currently FDA approved. Disulfiram and acamprosate help to avoid drinking and naltrexone reduces reward-associated effects, albeit with substantial side effects and with only mild effectiveness for treatment of AUD. The unexpected observation that the GLP-1 agonist semaglutide reduces alcohol consumption in rodents (Aranas et al., 2023, Chuong et al., 2023, Jerlhag, 2020) points to the re-examination of ethanol metabolism as a target of therapy. Semaglutide is believed to act primarily on receptors in the pancreas to increase circulating levels of GLP-1 although it has also been shown to stimulate GABA production by activating GAD (Wang et al., 2007) or by modulating GABA transmission (Chuong et al., 2023). Studies of GLP-1-regulated feeding behaviors have identified GLP-1 receptors in specific neurons in brain (Lockie, 2013, Sisley et al., 2014, Huang et al., 2022) including the ventral tegmental area (Alvarez et al., 2005, Merchenthaler et al., 1999). Evidence supporting its potential involvement in AUD comes largely from a genetic analysis that identified a non-synonymous SNP in GLP1R
