In RXR null mice L-FABP levels are dramatically reduced compared to wild-type animals [107]. L-FABP is a PPARα target gene and is necessary for the transport of fatty acids. Ethanol feeding increases hepatic FFA levels both in wild-type and null mice; however in RXR null mice L-FABP is not induced by ethanol and this effect is associated with accumulation of FFA and ethanol induced liver damage [107]. A recent paper from Razny et al. further demonstrated the RXR specific role on lipid metabolism and angiogenesis. Microarray studies on RXRα deficient mice fed with a high-fat diet for 7 weeks demonstrated a down-regulation of genes related to angiogenesis, whereas genes involved in adipogenesis, apoptosis, and inflammation were upregulated. Based on these results Razny et al. suggested that impaired fatty acid metabolism in liver leads to impaired angiogenesis due to lipotoxicity and promotion of adipogenesis [119].
