**2.2 Dietary chylomicrons**

The contribution of dietary fat, in form of chylomicron remnants or chylomicronderived spillover non-esterified fatty acids (NEFA), to liver fat accumulation depends on the amount and frequency of fat intake [29]. Chylomicron-derived TG is hydrolysed by lipoprotein lipase and mainly took up by adipose tissue, the rest of which is absorbed into the liver either by the LDL receptor (LDLR) or by the LDLR-related protein 1 (LRP1) [13, 30]. Once absorbed in the liver, chylomicron is hydrolysed by hepatic lysosomes to release FAs. In both obesity and NAFLD, hepatic expression of LDLR and LRP1 could be downregulated, which might be associated with the higher plasma concentrations of TG in these patients. Therefore, hepatic expression of LDLR and LRP1 participate in modulating the dyslipidemia and in preventing oxidized LDL-mediated liver injury.
