SLC2A12 and metabolic dysfunction-associated steatotic liver disease: A study by DeBosch et al. (2014) measured reduced fructose uptake in hepatocytes of GLUT8 knock-out mice, which protected the mice from fructose-induced intrahepatic lipid accumulation (steatosis), a key mechanism in the pathogenesis of NAFLD (DeBosch et al., 2014).