Liver-specific cholesteryl ester hydrolase deficiency attenuates sterol elimination in the feces and increases atherosclerosis in ldlr-/- mice.

ABSTRACT:

Objective

Liver is the major organ responsible for the final elimination of cholesterol from the body either as biliary cholesterol or as bile acids. Intracellular hydrolysis of lipoprotein-derived cholesteryl esters (CEs) is essential to generate the free cholesterol required for this process. Earlier, we demonstrated that overexpression of human CE hydrolase (Gene symbol CES1) increased bile acid synthesis in human hepatocytes and enhanced reverse cholesterol transport in mice. The objective of the present study was to demonstrate that liver-specific deletion of its murine ortholog, Ces3, would decrease cholesterol elimination from the body and increase atherosclerosis.

Approach and results

Liver-specific Ces3 knockout mice (Ces3-LKO) were generated, and Ces3 deficiency di

SUBMITTER: Bie J 

PROVIDER: S-EPMC3819806 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature