Liver X receptors (Lxrs) are master regulators of cholesterol catabolism, driving the elimination of cholesterol from the periphery to the lumen of the intestine. Development of pharmacological agents to activate Lxrs has been hindered by synthetic Lxr agonists' induction of hepatic lipogenesis and hypertriglyceridemia. Elucidating the function of Lxrs in regulating enterocyte lipid handling might identify novel aspects of lipid metabolism that are pharmacologically amenable. We took a genetic approach centered on the single Lxr gene nr1h3 in zebrafish to study the role of Lxr in enterocyte lipid metabolism. Loss of nr1h3 function causes anticipated gene regulatory changes and cholesterol intolerance, collectively reflecting high evolutionary conservation of zebrafish Lxra function. Intestinal nr1h3 activation delays transport of absorbed neutral lipids, with accumulation of neutral lipids in enterocyte cytoplasmic droplets. This delay in transport of ingested neutral lipids protects animals from hypercholesterolemia and hepatic steatosis induced by a high-fat diet. On a gene regulatory level, Lxra induces expression of acsl3a, which encodes acyl-CoA synthetase long-chain family member 3a, a lipid droplet-anchored protein that directs fatty acyl chains into lipids. Forced overexpression of acls3a in enterocytes delays, in part, the appearance of neutral lipids in the vasculature of zebrafish larvae. Activation of Lxr in the intestine cell-autonomously regulates the rate of delivery of absorbed lipids by inducting a temporary lipid intestinal droplet storage depot. Liver X receptors (Lxrs) are master regulators of cholesterol catabolism, driving the elimination of cholesterol from the periphery to the lumen of the intestine. Development of pharmacological agents to activate Lxrs has been hindered by synthetic Lxr agonists' induction of hepatic lipogenesis and hypertriglyceridemia. Elucidating the function of Lxrs in regulating enterocyte lipid handling might identify novel aspects of lipid metabolism that are pharmacologically amenable. We took a genetic approach centered on the single Lxr gene nr1h3 in zebrafish to study the role of Lxr in enterocyte lipid metabolism. Loss of nr1h3 function causes anticipated gene regulatory changes and cholesterol intolerance, collectively reflecting high evolutionary conservation of zebrafish Lxra function. Intestinal nr1h3 activation delays transport of absorbed neutral lipids, with accumulation of neutral lipids in enterocyte cytoplasmic droplets. This delay in transport of ingested neutral lipids protects animals from hypercholesterolemia and hepatic steatosis induced by a high-fat diet. On a gene regulatory level, Lxra induces expression of acsl3a, which encodes acyl-CoA synthetase long-chain family member 3a, a lipid droplet-anchored protein that directs fatty acyl chains into lipids. Forced overexpression of acls3a in enterocytes delays, in part, the appearance of neutral lipids in the vasculature of zebrafish larvae. Activation of Lxr in the intestine cell-autonomously regulates the rate of delivery of absorbed lipids by inducting a temporary lipid intestinal droplet storage depot. Atherosclerotic cardiovascular disease is the leading cause of death worldwide (1Lozano R. Naghavi M. Foreman K. Lim S. Shibuya K. Aboyans V. Abraham J. Adair T. Aggarwal R. Ahn S.Y. et al.Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010.Lancet. 2012; 380: 2095-2128Abstract Full Text Full Text PDF PubMed Scopus (9879) Google Scholar). Elevated serum cholesterol is a major causal risk factor for development and progression of atherosclerosis (2Kannel W.B. Dawber T.R. Friedman G.D. Glennon W.E. McNamara P.M. Risk factors in coronary heart disease: an evaluation of several serum lipids as predictors of coronary heart disease: the Framingham Study.Ann. Intern. Med. 1964; 61: 888-899Crossref PubMed Scopus (350) Google Scholar). The most widely used treatment for atherosclerosis is statin drugs, which potently inhibit 3-hydroxy-3-methylglutaryl CoA reductase, the rate-limiting enzyme of cholesterol biosynthesis (3Baigent C. Blackwell L. Emberson J. Holland L.E. Reith C. Bhala N. Peto R. Barnes E.H. Keech A. Simes J. et al.Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials.Lancet. 2010; 376: 1670-1681Abstract Full Text Full Text PDF PubMed Scopus (4534) Google Scholar). Nevertheless, statins do not fully mitigate cardiovascular risk. Recent epidemiological investigations reveal that postprandial (nonfasting) plasma lipid levels are a major determinant of cardiovascular risk because they reflect the persistence of highly atherogenic remnant lipoprotein particles in the circulation (4Jørgensen A.B. Frikke-Schmidt R. Nordestgaard B.G. Tybjærg-Hansen A. Loss-of-function mutations in APOC3 and risk of ischemic vascular disease.N. Engl. J. Med. 2014; 371: 32-41Crossref PubMed Scopus (636) Google Scholar). Statin drugs do not modulate the abundance or atherogenicity of remnant lipoprotein particles (5Varbo A. Benn M. Nordestgaard B.G. Remnant cholesterol as a cause of ischemic heart disease: evidence, definition, measurement, atherogenicity, high risk patients, and present and future treatment.Pharmacol. Ther. 2014; 141: 358-367Crossref PubMed Scopus (136) Google Scholar). Elucidation of the regulatory events controlling the pace of entry of ingested lipids into the blood stream in chylomicrons might afford the opportunity to blunt postprandial hyperlipidemia. Human jejunal biopsies (6Robertson M.D. Parkes M. Warren B.F. Ferguson D.J.P. Jackson K.G. Jewell D.P. Frayn K.N. Mobilisation of enterocyte fat stores by oral glucose in humans.Gut. 2003; 52: 834-839Crossref PubMed Scopus (124) Google Scholar), prolonged, label-free lipid droplet imaging of live loops of mouse intestine (7Zhu J. Lee B. Buhman K.K. Cheng J-X. A dynamic, cytoplasmic triacylglycerol pool in enterocytes revealed by ex vivo and in vivo coherent anti-Stokes Raman scattering imaging.J. Lipid Res. 2009; 50: 1080-1089Abstract Full Text Full Text PDF PubMed Scopus (124) Google Scholar), and fluorescent lipid probe-based visualization of intestinal lipid droplets in zebrafish larvae (8Carten J.D. Bradford M.K. Farber S.A. Visualizing digestive organ morphology and function using differential fatty acid metabolism in live zebrafish.Dev. Biol. 2011; 360: 276-285Crossref PubMed Scopus (83) Google Scholar) have revealed that a substantial fraction of absorbed lipids remain in the enterocyte for many hours following a meal. These findings suggest that there is an intrinsic mechanism for delaying, in part, transit of absorbed lipids. The molecular mechanism accounting for this hours-long retention of absorbed lipids in the intestine is not known. Liver X receptors (Lxrs) are nuclear receptor transcription factors that regulate energy metabolism through engaging specific metabolite substrates such as oxysterols and then altering the expression of diverse, but functionally integrated genes (9Gabbi C. Warner M. Gustafsson J-Å. Action mechanisms of liver X receptors.Biochem. Res. 2014; PubMed Scopus Google of metabolism by the nuclear receptors and Biol. 2012; PubMed Scopus Google Scholar). Lxrs are of cholesterol (9Gabbi C. Warner M. Gustafsson J-Å. Action mechanisms of liver X receptors.Biochem. Res. 2014; PubMed Scopus Google of metabolism by the nuclear receptors and Biol. 2012; PubMed Scopus Google Scholar). genes of Lxr factors in cholesterol lipoprotein cholesterol and and triacylglycerol glucose and and (9Gabbi C. Warner M. Gustafsson J-Å. Action mechanisms of liver X receptors.Biochem. Res. 2014; PubMed Scopus Google of metabolism by the nuclear receptors and Biol. 2012; PubMed Scopus Google Scholar). Lxr have been in Lxra is in in lipid metabolism is more widely (9Gabbi C. Warner M. Gustafsson J-Å. Action mechanisms of liver X receptors.Biochem. Res. 2014; PubMed Scopus Google of metabolism by the nuclear receptors and Biol. 2012; PubMed Scopus Google Scholar). Lxra activation cholesterol and of cholesterol to role in cholesterol Lxra hepatic and liver and blood triacylglycerol levels J. B. of mouse regulatory gene by and PubMed Scopus Google A. L. S. S. M. et of in of PubMed Scopus Google A. T. T. et of lipogenesis by pharmacological activation of the liver X receptor to of lipoprotein Biol. Full Text Full Text PDF PubMed Scopus Google J. M. S.A. Liver expression is for cholesterol and cholesterol transport in 2012; PubMed Scopus Google Scholar), of which are risk for cardiovascular disease S. fatty liver disease and cardiovascular disease: has the for to 2012; PubMed Scopus (83) Google Scholar). This driving elimination of cholesterol liver has been a major to have Lxra regulates intestinal and has as a major for metabolism A. The of zebrafish to PubMed Scopus Google Scholar). many such as and of retention of the protein gene in zebrafish has to L. Lee S. vivo visualization and of lipid accumulation in 2011; PubMed Scopus Google L. R. K. J. T. et and in zebrafish larvae a high cholesterol Biol. 2010; Full Text Full Text PDF PubMed Scopus Google K. L. K. C. J. J. et lipid lipoprotein and lipid in Res. 2009; PubMed Scopus Google Scholar). development K. McNamara A. et lipid for the of of Lipid Res. 2012; Full Text Full Text PDF PubMed Scopus Google Scholar). have a of serum and metabolite to study lipid metabolism A. protein is for lipid and of lipids in zebrafish PubMed Scopus Google L. S. A. A for of 2012; PubMed Scopus Google S. K. A. fatty are of cholesterol PubMed Scopus Google Scholar). to this zebrafish have a single Lxr A. A. Gustafsson J-Å. and expression of liver X receptor in zebrafish.Dev. PubMed Scopus Google L. M. expression and of liver X receptor transcription factors of and B. 2009; PubMed Scopus Google S. B. R. L. A. M. R. et novel by of nuclear receptor PubMed Scopus Google Scholar), which is to Lxra L. M. expression and of liver X receptor transcription factors of and B. 2009; PubMed Scopus Google Scholar). This to the of in development and lipid that in Lxr family L. K. S. Gustafsson Liver X receptors in the from lipid to PubMed Scopus Google Scholar). We that Lxra activation causes retention of absorbed neutral lipids in This delay in lipids to the circulation from high-fat hypercholesterolemia and hepatic On a molecular level, Lxra induces expression of that the absorbed lipids to cytoplasmic lipid droplets and from and the Lxra gene acyl-CoA synthetase long-chain family member which encodes a lipid droplet-anchored long-chain acyl-CoA synthetase that is to the and of lipid droplets M. B. C. R. M. C. R. J. The of acyl-CoA synthetase is for the on lipid droplets and the function in fatty acid Lipid Res. 2012; Full Text Full Text PDF PubMed Scopus Google A. A. A. M. A. M. C. et synthetase lipid droplet in Biol. PubMed Scopus Google T. J. M. S. M. A. et of in of neutral lipids in cytoplasmic lipid droplets in Lipid Res. 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