Effect of Cholesterol-Lowering Variants in ANGPTL3 and APOB Genes on Liver Disease

Recently, new lipid-lowering drugs have become available that act by reducing hepatic very low–density lipoprotein production because of the inhibition of apolipoprotein B and angiopoietin-like 3 function.1 Impaired very low–density lipoprotein secretion may lead to liver steatosis, thus raising worry about the long-term hepatic safety of these medications. Hereby, we aimed to investigate the hepatic consequences of the presence of rare inactivating variants in the APOB and ANGPTL3 genes used as genetic instruments to mimic the action of new low-density lipoprotein cholesterol (LDL-C)-lowering medications in the large cohort of UK Biobank individuals.