RNA-Seq of liver from CLA-exposed mice with/without PPARa antagonist

We demonstrate that conjugated linoleic acid (CLA), when given to mice as a dietary supplement, induced an enlarged liver and hepatic steatosis. The progression of NAFLD and insulin resistance was reversed by GW6471 a small-molecule antagonist of PPARa. Transcriptional profiling of livers unraveled that genes involved in lipid metabolism core gene programs controlled by PPARa in response to CLA and GW6471.Our findings reveal a novel role of PPARa in the regulation of lipid homeostasis and highlight its druggable nature in NAFLD. Overall design: Hepatic mRNA profiles of mice treated with CLA or PPARa antagonist or CLA combined PPARa antagonist