Abstract
Background and Aims : Lysosomal acid lipase (LAL) catalyzes the hydrolysis of cholesteryl esters and triglycerides in the lysosomal compartment. Recently, it was shown that NAFLD patients can develop an acquired LAL deficiency which is rescued by PPAR-alpha activation. Aim of the study was to investigate the role of other isoform-specific and dual PPAR agonists on lipid accumulation and LAL activity using an in vitro model of steatosis.
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