Carnitine palmitoyl transferase 1A (CPT-1A) catalyzes the transfer of the acyl group of long-chain fatty acid-CoA moiety onto carnitine, an essential step for the uptake of long-chain fatty acids and their subsequent beta-oxidation in the mitochondrion. It is the rate-limiting step in beta-oxidation and is highly expressed in the liver where it plays an important role in triglyceride metabolism. The physiological consequences of CPT-1A deficiency in liver, however, are yet to be reported. In this study, we have generated mouse model with liver specific deletion of CPT-1A gene. We found that deletion of CPT-1A in liver caused an increased triglyceride content in liver and decreased epididymal adipose tissue weight compared with control mice under high fat diet feeding conditions. RNA-seq analysis between livers of CPT-1A knockout vs. wild type mice revealed altered expression of many metabolic pathways such as steroid hormone biosynthesis and PPAR signaling pathways as well as some novel hepatokines. Further analysis of the significance of these changes is under way but the data so far suggest that a pharmacological agent that alters hepatic fatty acid oxidation (perhaps acting on CPT-1A) could provide a novel approach to target nonalcohol fatty liver disease (NAFLD).


D. Wu: None.

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