(26), and recent studies have shown that it regulates brain specific functions related to alcohol consumption in mice. For example, mice lacking brain expressed Klb showed increased ethanol preference (15). Furthermore, FGF21 was found to suppress ethanol consumption in wild-type mice but had no effect on mice lacking Klb in the brain. Previous studies have shown that FGF21 and KLB are involved in sweet and alcohol preference in mice (27), and a recent study in humans found increased FGF21 expression in blood after binge drinking (28). These findings suggest that KLB and FGF21 act as part of a brain-liver endocrine axis that regulates alcohol consumption. Future studies could explore the effects of analogues of FGF21 on alcohol consumption, which are currently being tested in clinical trials for the treatment of type 2 diabetes and obesity (29). Although KLB and FGF21 seem to be promising avenues for translational research, it is worth noting that while SNPs in KLB are associated with alcohol consumption, they have not yet shown any association with AUD (12, 18). This implies that this system might only be relevant for the regulation of normative consumption, although studies of larger AUD populations may yet reveal a role for
