Human and animal studies associated treatments with GLP1 receptor agonists to amelioration of hepatic fat accumulation, insulin resistance and increase of FAs β-oxidation in NAFLD,43–47 while in ALD only an effect to reduce ethanol intake was demonstrated both in rodents and humans.48 GLP-1 colonic expression can be modulated by bile acids (i.e. deoxycholic and lithocholic acid) via TGR5, or by bacterial derived short chain fatty acids (SCFAs) via GPR43.38,49 In our experiments we found that ethanol reduced expression of both TGR5 and GPR43, which were restored by Bt supplementation. This evidence concerns the gene GLP1R and metabolic dysfunction-associated steatotic liver disease.