GRM5 and Hepatic steatosis: These responses result in reduced fatty acid oxidation and enhanced hepatic lipogenesis.6 Several animal experiments have established that chronic alcohol consumption could exacerbate alcoholic fatty liver by triggering abnormal CB1R-mediated signaling.7,10 However, the authors’ recent studies have clearly demonstrated that chronic alcohol consumption induces oxidative stress-mediated glutamate excretion from hepatocytes, which triggers the activation of mGluR5 to produce 2-AG, but not AEA, in HSCs via DAGL-beta.