MLXIPL and fatty liver disease: Fru and Glc contribute to liver steatosis both delivering substrates for fatty acids (FAs) and TAGs synthesis (acetyl-CoA and glycerol molecules, respectively) and inducing transcription factors (sterol regulatory element-binding protein-1c—SREBP-1c and carbohydrate-responsive element-binding protein—ChREBP) which enhance lipid synthetic pathways [35].