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 associated with AUD (Suchankova et al., 2015). The use of semaglutide to reduce alcohol consumption lacks rigorous clinical evidence, and it may rely on mechanisms outside the brain and/or utilize non-metabolic pathways. However, we speculate that it may represent a novel therapeutic strategy. With evidence that ethanol interferes with neuronal metabolism, potentially affecting excitability, and the observation that a presumed metabolic modulator reduces drinking behavior, there is ample reason to investigate this regulatory network further, with an eye towards developing therapies for those suffering from AUD.
