Hepatic NPC1L1 promotes hyperlipidemia in LDL receptor deficient mice

L1-Tg/LDLR−/− mouse is a humanized model to study cholesterol absorption and transportation. The results obtained from L1-Tg/LDLR−/− mouse indicated no feedback mechanism to inhibit NPC1L1 function in liver and hepatic expression of NPC1L1 correlated with VLDL secretion in hypercholesterolemia state.