1 Vagelos College of Physicians and Surgeons of Columbia University, New York, NY.
Non alcoholic fatty liver disease (NAFLD) occurs in 25-40% of the US and European populations, with rates up to 70% in individuals with diabetes mellitus. The majority of people with NAFLD also have hypertriglyceridemia, characterized by increased secretion of very low density lipopoproteins (VLDL) carrying triglycerides (TG) (1). This raises several questions: Why would there be both increased secretion of VLDL and increased hepatic fat content? If VLDL TG secretion cannot keep up with TG synthesis, why isn't there a compensatory increase in hepatic fatty acid oxidation? What determines whether TG synthesized within the bilayer membrane of the endoplasmic reticulum (ER) moves to the cytoplasm as lipid droplets (LDs) or into the ER lumen, where it can be incorporated into VLDL?.