Fig 8. Schematic of role of EL in TRL catabolism.

A-B. In the setting of EL expression (A), phospholipid lipolysis on TRL in postprandial or high fat-fed state allows for synergistic and efficient TG lipolysis by LPL, which promotes FA and TRL remnant uptake by the liver. Multiple FAs including long chain PUFAs are internalized by the liver. In EL-deficient mice (B), lipolysis of phospholipids on the outer shell of TRLs is impaired, resulting in less efficient access of LPL to TRL TGs and reduced TG lipolysis and remodeling of TRLs to smaller remnants, thus reducing TRL remnant uptake by the liver. In addition, the lack of ability of EL to catalyze lipolysis of phospholipids containing its preferred substrates of long chain PUFAs results in decreased PUFA uptake by the liver.