Other mechanisms such as alterations in triglyceride secretion by liver cells due to malfunction of lipoproteins, and hyperglycemia-induced hepatic upregulation of GLUT2, which transports excess sugar from the blood into the liver and converted into excess fat, have been suggested as contributory factors in the development of NAFLD and NASH in diabetic patients [73]. Here, SLC2A2 is linked to metabolic dysfunction-associated steatotic liver disease.