Conversely, overexpression of nr1h3 in enterocytes confers protection from dyslipidemia and hepatic steatosis when animals are fed a HFD; this metabolically beneficial effect of nr1h3 overexpression is due to the induction of a transcriptional program resulting in temporary enterocyte storage of lipids, delaying an en masse delivery of atherogenic lipoprotein particles in the circulation. This evidence concerns the gene NR1H3 and fatty liver disease.