NUTRITION AND METABOLISM: Edited by Frank M. Sacks and Majken K. JensenDietary fructose and dyslipidemia: new mechanisms involving apolipoprotein CIIIHieronimus, Bettina; Stanhope, Kimber L.Author Information Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, California, USA Correspondence to Kimber L. Stanhope, Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA. Tel: +1 530 752 3720; fax: +1 530 752 2474; e-mail: email@example.com Current Opinion in Lipidology: February 2020 - Volume 31 - Issue 1 - p 20-26 doi: 10.1097/MOL.0000000000000653 Buy Metrics Abstract Purpose of review Chronic consumption of fructose and fructose-containing sugars leads to dyslipidemia. Apolipoprotein (apo) CIII is strongly associated with elevated levels of triglycerides and cardiovascular disease risk. We reviewed the effects of fructose consumption on apoCIII levels and the role of apoCIII in fructose-induced dyslipidemia. Recent findings Consumption of fructose increases circulating apoCIII levels compared with glucose. The more marked effects of fructose compared with glucose on apoCIII concentrations may involve the failure of fructose consumption to stimulate insulin secretion. The increase in apoCIII levels after fructose consumption correlates with increased postprandial serum triglyceride. Further, RNA interference of apoCIII prevents fructose-induced dyslipidemia in nonhuman primates. Increases in postprandial apoCIII after fructose, but not glucose consumption, are positively associated with elevated triglycerides in large triglyceride-rich lipoproteins and increased small dense LDL levels. Summary ApoCIII might be causal in the lipid dysregulation observed after consumption of fructose and fructose-containing sugars. Decreased consumption of fructose and fructose-containing sugars could be an effective strategy for reducing circulating apoCIII and subsequently lowering triglyceride levels. Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.